Good afternoon. This is Scott Wolchko, President and CEO of Fate Therapeutics, and thank you all for joining us. We are excited to share with you today interim phase I clinical data for our FT516 and FT596 off-the-shelf iPSC-derived NK cell programs in relapsed/ refractory B-cell lymphoma. Please note, as we discuss our FT516 and FT596 programs today, our comments will include forward-looking statements that involve risks and uncertainties. These risks and uncertainties are detailed in our SEC filings, and I refer you to our most recent Form 10-Q filed with the SEC for full disclosure of these factors. Note that undue reliance should not be placed on forward-looking statements which speak only as of the date they are made, as the facts and circumstances underlying these forward-looking statements may change. Joining me on today's call are Dr. Wayne Chu, our Senior Vice President of Clinical Development, Dr. Sarah Cooley, our Senior Vice President of Clinical Translation, and Dr. Bob Valamehr, our Chief Research and Development Officer. During our discussion, we will review interim clinical data from our ongoing FT516 study in relapsed/ refractory B-cell lymphoma, including sharing a first look at durability of response. Additionally, we will review interim clinical data from our ongoing FT596 study in relapsed/ refractory B-cell lymphoma, including sharing response rates after a single-dose treatment cycle. Finally, we will review selected translational observations that differentiate our off-the-shelf iPSC-derived NK cell franchise and demonstrate its unique potential to change the field of cell-based cancer immunotherapy. Ed Dulac, our Chief Financial Officer, will be monitoring for questions that we will address at the conclusion of the prepared presentation. FT516 is our off-the-shelf NK cell product candidate derived from a clonal master induced pluripotent stem cell line engineered with a novel high-affinity non-cleavable CD16 Fc receptor. CD16 is an activating receptor that is naturally expressed on NK cells and mediates antibody-dependent cellular cytotoxicity, or ADCC, a potent anti-tumor mechanism by which NK cells can recognize, bind, and kill antibody-coded cancer cells. Our proprietary hnCD16 Fc receptor has been specifically modified to maximize ADCC by preventing CD16 downregulation and by binding more effectively to tumor-targeting antibodies for enhanced anti-tumor activity. FT596 is our first multiplexed engineered iPSC-derived CAR-NK cell product candidate. FT596 builds upon FT516 and incorporates both the hnCD16 Fc receptor and a novel CD19-targeted chimeric antigen receptor, which has been specifically optimized for NK cell biology. These two receptors enable multi-antigen targeting of tumor cells, a differentiated approach that is intended to uniquely address tumor heterogeneity and overcome antigen escape. We believe multi-antigen targeting has the potential to drive deeper, more durable responses for patients, including in patients that might not effectively be treated with single-antigen targeting modalities such as monoclonal antibodies, bispecific engagers, and CAR T-cell therapies. FT596 is also our first product candidate to incorporate our novel IL-15 receptor fusion, which is designed to promote NK cell survival and anti-tumor activity. Both FT516 and FT596 are available off the shelf and both product candidates are designed to be delivered to patients in the outpatient setting. As we review clinical data today from our studies, it is important to note, though, some key differences in the current FT516 and FT596 treatment regimens. First off, dosing. With FT516, three doses are administered within a 28-day treatment cycle. These three doses are administered on days 1, 8, and 15. In contrast, with FT596, only a single- dose is administered on day 1. Secondly, cytokine support. Each dose of FT516 is administered with low-dose IL-2 to promote NK cell activity. FT596 is not aided by co-administration of IL-2 and relies on its IL-15 receptor fusion to drive activity. Thirdly, cycles. FT516 is administered over two cycles, while FT596 is administered over one cycle. Up to six doses of FT516, compared to only one dose of FT596, are delivered to patients. Patients who derive clinical benefit from the first FT596 cycle may receive a second single-dose cycle with FDA consent. Finally, rituximab. While FT516 is combined with rituximab to exploit its hnCD16 receptor-enhanced ADCC, the FT596 study has two treatment regimens. A monotherapy arm that evaluates the single antigen targeting activity of the product candidate's novel CD19-targeted CAR receptor, and a combination arm that combines FT596 with rituximab to exploit the product candidate's multi-antigen targeting functionality. Shown here is the total cell dose of FT516 and FT596 delivered in one 28-day treatment cycle. As we think about today's FT596 clinical data, we look to the monotherapy arm to assess the potential of our novel CD19-targeted CAR construct to drive responses, particularly in those patients that are naive to autologous CD19 CAR T-cell therapy. As we consider the combination arm, it is important to recall that dose dependency observations from our FT516 study, where the activity of the hnCD16 construct was first observed at 90 million cells per dose, delivered as three weekly doses. In other words, a total cell dose of 270 million FT516 cells. Based on these observations, we would not expect the hnCD16 construct to be a major contributor to efficacy at single- dose levels of 30 million and 90 million FT596 cells. We also consider the first 10 patients treated with the combination arm to primarily be a test of the CAR construct's activity, rather than a rigorous assessment of the multi-antigen targeting functionality of FT596. Here's our first look at FT516 durability. At the ASCO annual meeting in June, we presented positive interim clinical data for 11 patients treated in the second and third FT516 dose cohorts of 90 million cells per dose and 300 million cells per dose, respectively. Eight of 11 patients, or 73%, achieved an objective response, including six patients who achieved a complete response on day 29, following the second FT516 treatment cycle. Notably, two of four patients previously treated with autologous CD19-targeted CAR T-cell therapy achieved a complete response. We are pleased to share today that at three months from the first infusion, all eight responders maintained their response without further therapeutic intervention. As of the data cutoff date of July 7, 2021, five of 11 patients, or 45%, continued in ongoing response without further therapeutic intervention. This includes four patients that remain in complete response at 4.6- 9.5 months, and one patient that remain in partial response at 6.1 months. The favorable safety profile, high response rates, and durability of response of FT516, including in patients that have progressed through multiple CD20-targeted regimens, demonstrate the unique therapeutic value of our proprietary hnCD16 receptor, and in combining FT516 with rituximab. I'm also pleased to share today early clinical data from our FT596 clinical trial. As of June 25, 2021 data cutoff, 10 patients in the monotherapy arm and 10 patients in the combination arm, so 20 patients total, were evaluable for safety and efficacy in the first, second, and third single- dose cohorts of 30 million, 90 million, and 300 million cells respectively. In the second and third single- dose cohorts, comprising a total of 14 patients, 10 of 14 patients or 71%, achieved an objective response, including seven patients or 50%, that achieved a complete response as assessed on day 29 following FT596 infusion. Eight of 10 patients, or 80%, that had not previously received CD19-targeted CAR T-cell therapy achieved an objective response, including five patients that achieved complete response. Two of four patients that previously received CD19-targeted CAR T-cell therapy achieved a complete response, both of whom were treated in the combination arm, once again underscoring the potential therapeutic value of multi-antigen targeting to overcome antigen escape. Notably, of the six patients in dose cohort 1 across both arms, only one of six patients achieved an objective response. In contrast, six patients in dose cohort 3 across both arms, five of those six, or 83%, achieved an objective response, suggesting a dose-response relationship for FT596. The observed safety profile of FT596 was favorable and potentially differentiated from that of T-cell modalities. We believe these early FT596 clinical data are exciting. Again, I want to emphasize that this is a CAR T-cell-like treatment paradigm. Cy/Flu, followed by a single- dose of FT596, with initial response assessment conducted at one month following infusion. As a whole, the interim clinical data from our FT516 and FT596 studies are compelling and demonstrate a safety profile, response rate, and durability of response that support the disruptive potential of our engineered off-the-shelf iPSC-derived NK cell programs for patients with relapsed/ refractory lymphoma. I will now turn it over to Wayne for a more detailed review of our clinical data. Thanks, Scott. Beginning with a quick reminder on the FT516 study design. As Scott mentioned, FT516 is administered in up to two treatment cycles. Each cycle consists of 3 consecutive days of Flu/Cy conditioning, a single- dose of rituximab, and three weekly doses of FT516. IL-2 cytokine support is administered with each FT516 dose. Of note, there is no requirement for mandatory hospitalization during the treatment period. All treatments may be administered in the outpatient setting. Baseline characteristics are summarized here for the 13 patients treated in the first three- dose cohorts. These characteristics are typical of a patient population with advanced relapsed/ refractory lymphoma, where treatment options are extremely limited. In this regard, several disease-specific characteristics to note here as we consider response rates and durability of response. First, 10 patients had aggressive histology, including diffuse large B-cell lymphoma, high-grade B-cell lymphoma, and transformed indolent lymphoma. Three patients had double-hit or triple-hit lymphoma that are known to be associated with particularly poor clinical outcome. Six patients were refractory, meaning no response to their most recent prior treatment, and five patients received prior CD19-targeted CAR T-cell therapy. Finally, most patients had advanced stage disease with substantial tumor burden. Here, we show individual patient histories and response rates for the 11 patients treated in the second and third dose cohorts of 90 million cells per dose and 300 million cells per dose, respectively. As I mentioned, six patients were refractory to their most recent prior therapy, and for nearly all of the five patients that responded to their most recent prior therapy, the duration of response was very short. In fact, of the 11 patients treated with FT516 in the second and third dose cohorts, only two responded to their most recent prior therapy with a duration of response exceeding 2 months. FT516 response assessment conducted after cycle 2 show that eight of the 11 patients had an objective response as assessed by Lugano 2014 criteria. Of note, six of these objective responses were complete responses, demonstrating the ability of FT516 to drive clinically meaningful responses. Also of note, two of four patients that had received prior CD19-targeted CAR T-cell therapy achieved an objective response, both of which were complete responses. Updated safety data for FT516 is summarized in this slide, which overall continue to support a highly favorable safety and tolerability profile, and one that is differentiated from T-cell based modalities. There were no cases of any grade of CRS, ICANS, which is immune cell associated neurotoxicity syndrome, or GVHD, and there were no FT516 related serious adverse events, and no FT516 related grade 3 or greater adverse events. Overall, the data support administration of FT516 in the outpatient setting. In fact, over 85% of FT516 doses to date were administered in the outpatient setting. FT516 durability of response is illustrated in the swim lane plot of the 11 patients treated in the second and third dose cohorts. Of the 8 patients that responded to FT516, all eight patients maintained their response at three months from first infusion. This indicates a 73% overall response rate and a 55% complete response rate at month 3, which is shown by the vertical dotted line. As of the July 7, 2021 data cutoff, five patients continue an ongoing response ranging from 4.6-9.5 months, four of whom continue in complete response. This includes three patients with aggressive lymphomas, subjects 2011, 2013 and 2015, all three of whom were refractory to their most recent prior therapy, and one of whom, subject 2015, had previously been treated with a CD19-directed CAR T-cell therapy. The ability of FT516 to provide profound clinical benefit in extremely difficult to treat lymphoma patients is exemplified in this case study of patient 2015, who was featured in our ASCO presentation. This patient had an aggressive refractory high-grade triple-hit B-cell lymphoma characterized by bulky disease, which was refractory to all prior therapies, with the exception of autologous CD19 CAR T-cell therapy, for which the duration of response was extremely short. Upon treatment with FT516, the patient achieved a complete response, and the patient continues in complete response at almost five months. As of the most recent follow-up, the patient was assessed as being MRD negative by local testing with the clonoSEQ assay, suggestive of a very deep response with the potential for long-term durability. Overall, we remain highly encouraged by the data with FT516. The safety profile, response rate, and durability of response demonstrate that FT516 can be effectively combined with CD20-targeted monoclonal antibody to drive meaningful therapeutic benefit in difficult-to-treat patients, including those with aggressive lymphomas, with refractory disease, and with disease progression following autologous CD19-targeted CAR T-cell therapy. With that, I will now turn it over to Bob to review the biologic features and preclinical data of FT596. Thanks, Wayne. As described earlier by Scott, FT596 is an off-the-shelf multi-antigen targeted iPSC-derived NK cell that incorporates three novel anti-tumor modalities. First, a novel high-affinity non-cleavable CD16 Fc receptor to maximize ADCC in combination with various therapeutic antibodies. Second, a unique IL-15/IL-15 receptor fusion to promote NK cell survival, proliferation, and anti-tumor activity, avoiding the need for exogenous cytokine support. Three, a novel CAR optimized for NK cell activity that targets CD19. Next slide. Because FT596 is manufactured from a clonal master engineered iPSC line, the FT596 drug product is a pure population of NK cells that uniformly expresses its three engineered modalities. The manufacturing process is robust. Over 1 trillion iPSC-derived NK cells can be produced from a single vial of banked starting material. Note that these yields are based on our small-scale manufacturing process, and we are currently working to implement larger-scale processes as we launch our new GMP manufacturing facility. As seen here in this in vitro demonstration of multi-antigen targeting functionality of FT596 in eliminating a heterogeneous population of lymphoma cells. Isogenic lymphoma lines, which generated to either express both CD19 and CD20, as seen in red, or to only express CD20, as seen in green. These lines were combined in a 50/50 ratio and then co-cultured with no effector cells, a CAR NK cell targeting only CD19, or with FT596, which can leverage both its CAR and its hnCD16 Fc receptor to target CD19 and CD20. As illustrated, both CAR NK cells and FT596 clearly target the CD19-positive lymphoma compartment of the co-culture. Although you can see that IL-15 receptor fusion of FT596 further enhances killing to drive complete elimination of CD19-positive lymphoma cells. With the addition of rituximab, FT596 uniquely recognizes and kills CD20-positive lymphoma cells, as evidenced by the elimination of the CD19 negative, CD20 positive green population. Turning to slide 21. The anti-tumor activity of FT596 is highlighted here in various in vivo xenograft models of leukemia and lymphoma. On the left, effective CAR-mediated cytotoxicity is demonstrated as NALM-6 cells in red are eliminated by FT596 in green in this disseminated xenograft model of leukemia. On the right, the hnCD16 mediated cytotoxicity is shown using the aggressive Raji lymphoma xenograft model. Rituximab alone in blue failed to provide durable inhibition of tumor growth, whereas the combination of FT596 and rituximab in purple effectively clears all mice of the tumor burden. As these data demonstrate, we believe best-in-class cell products will have multi-antigen targeting functionality to address tumor heterogeneity and overcome antigen escape, driving deep and durable responses for patients. Now back to Wayne to discuss the FT596 study design and clinical results. Thanks, Bob. Turning now to our clinical data with FT596. The FT596 study has a monotherapy arm and a combination arm with rituximab. As Scott mentioned, there are some key differences in treatment with FT596 as compared to FT516. While FT516 is administered three times in a cycle with IL-2 cytokine support, only a single- dose of FT596 is administered, and it is administered without any exogenous cytokine support. Similar to FT516, there is no requirement for mandatory hospitalization during the FT596 treatment period, and all treatments may be administered in the outpatient setting. Today, we will describe clinical data from a total of 20 patients, 10 treated in the monotherapy arm and 10 treated in the combination arm at single-dose levels ranging from 30 million cells to 300 million cells. Patient baseline characteristics are summarized here. Similar to what was previously presented for the FT516 study, these characteristics are typical of a patient population with advanced relapse and refractory disease. Several things to note here as we consider response rates with FT596. Patients received a median of four prior lines of therapy, and seven of the 20 patients received prior CD19-directed CAR T-cell therapy. A full 50% of patients were refractory. As a reminder, these are patients that had no response to their last prior treatment. In comparing baseline characteristics between the monotherapy arm and the combination arm, it does appear, although data is early, that patients in the combination arm had more difficult-to-treat disease, as evidenced by the higher percentage of patients with aggressive histology, refractory disease, higher stage disease, and greater tumor burden. Individual patient histories and response rates for the seven patients treated in the second and third dose cohort of the monotherapy arm are presented here with a data cutoff date of June 25, 2021. Only two of these seven patients had documented response to last prior therapy. Response assessments conducted after a single- dose of FT596 show that six of seven patients had an objective response as assessed by Lugano 2014 criteria, including three complete responses. At this point, it is important to underscore that this response assessment is conducted at the end of the first cycle. This does not capture any potential benefit from retreatment with FT596. In other words, this is the patient-derived CAR T-cell-like treatment paradigm, one dose only. Of note, the one patient that failed to respond was previously treated with autologous CD19-targeted CAR T-cell therapy. For the six patients who are naive to CD19-targeted CAR T-cell therapy, the response rate was 100%, demonstrating the robust clinical activity of the product candidate's CAR construct. Safety data for the 10 patients treated in the monotherapy arm is summarized in this slide, which again supports a highly favorable safety and tolerability profile that is differentiated from T-cell modalities, including T-cell engagers as well as CAR T-cell therapies. With respect to adverse events of interest, there were no cases of any grade of CRS, ICANS, or GVHD. Additionally, there were no FT596-related serious adverse events, and there were no FT596-related Grade 3 or greater adverse events of interest. Of note, the events of infection were not attributed to FT596 by investigators and were generally reflective of the underlying disease and effects of conditioning chemotherapy. Individual patient histories and response rates for the seven patients treated in the second and third dose cohort of the combination arm are presented here with a data cutoff date of June 25, 2021. Only two of these seven patients had documented response to last prior therapy, one of which had very short duration of response of less than two months, again indicative of a very difficult-to-treat patient population. Response assessments conducted after a single- dose of FT596 combined with rituximab showed that four of the seven patients had a complete response as assessed by Lugano 2014 criteria. Notably, three patients that achieved a complete response were refractory to their most recent prior therapy. As we observed with FT516 in combination with rituximab, FT596 was also effective in driving complete responses in patients previously treated with CD19-targeted CAR T-cell therapy. In the combination arm, three of the seven patients were previously treated with CD19-targeted CAR T-cell therapy, with two of these three patients achieving a complete response. The ability of FT596 to provide clinical benefit in extremely difficult-to-treat lymphoma patients is exemplified in this case study of patient 2016. The patient had refractory diffuse large B-cell lymphoma and was treated with six prior therapies, including multiple CD20-targeted regimens, as well as autologous CD19-targeted CAR T-cell therapy. The patient tolerated FT596 well, with no events of any grade CRS, ICANS, or GVHD. With Grade 3 or greater treatment-emergent toxicities limited to hematologic cytopenia. Upon treatment with a single- dose of FT596, combined with a single- dose of rituximab, the patient achieved a complete response, exemplifying the activity of FT596 in patients who failed multiple standard therapies, including autologous CD19-directed CAR T-cell therapy. Safety data for the 10 patients treated in the combination arm is summarized in this slide, which, similar to the safety data for FT596 monotherapy, suggests a highly favorable safety and tolerability profile differentiated from T-cell-based modalities. The data also indicate that the safety and tolerability profile of FT596 is not adversely affected by the addition of rituximab. With respect to adverse events of interest, there were no cases of any grade of ICANS or GVHD. Additionally, the events of infection were not attributed to FT596 and again, were generally reflective of the underlying disease and effects of conditioning chemotherapy. There were two cases of low-grade CRS reported, one Grade 1 and one Grade 2, both of which resolved within 24 hours. Digging into these two CRS events a bit further, in the case of patient 2005, Grade 1 CRS was reported following administration of 30 million FT596 cells, characterized only by fever that resolved in the absence of any CRS-directed therapy on the same day of its onset. Of note, this patient had multiple concurrent factors that could potentially have contributed to the fever of presentation, including a history of lymphoma-related fever and disease-associated pleural effusions necessitating placement of an indwelling pleural catheter. In the case of patient 2011, Grade 2 CRS was reported following administration of 90 million FT596 cells and characterized by fever and hypotension. In this case, tocilizumab was empirically administered as CRS-directed therapy. Additionally, antibiotics were empirically administered for infection, which is known to have a similar clinical presentation as CRS. In this regard, the patient was subsequently confirmed to have a pneumonia by CT scan, and notably, the fever and hypotension resolved on the same day as onset. This slide summarizes the clinical activity of FT596 as monotherapy and in combination with rituximab. It is worth emphasizing that these responses reflect a single- dose of FT596 and do not capture the potential benefit of retreatment. In total, in those cohorts 2 and 3 at 90 million cells and 300 million cells respectively, 10 of 14 patients, or 71%, had an objective response, with seven patients, 50%, achieving a complete response. Among the 10 patients who are CD19 CAR T-cell naive, eight or 80%, had an objective response, with five, 50%, achieving a complete response. Finally, among the four patients who received prior CD19 CAR T-cell therapy, two or 50%, had an objective response, both of which were complete responses. Of note, there is strong indication of dose-dependent activity. Specifically, at the 30 million cell dose, only one of six patients achieved an objective response. While at the 300 million cell dose, five of six patients, 83%, achieved an objective response. While it's easy to focus on the patients whose disease responded to FT596 treatment, it is important to understand the underlying disease and clinical characteristics of those patients who did not respond to FT596. In this regard, observations from the four patients who did not respond when treated with 90 million FT596 cells or higher are summarized here. Notable observations include the following. In the monotherapy arm, which is reliant on CD19-targeted CAR construct and is not aided by the product candidate's hnCD16 receptor, the one non-responding patient had previously been treated with autologous CD19-targeted CAR T-cell therapy. In the combination arm, of the three patients that did not respond, one patient had previously been treated with both autologous CD19 CAR T-cell therapy and an investigational CD20-targeted CAR T-cell therapy. While the other two patients had aggressive lymphomas that were refractory or had extremely short durations of response to frontline therapy. We are further assessing non-responders and certainly believe the learnings will be critical as we seek to deliver clinically meaningful responses for all patients. As we have mentioned multiple times in this presentation, the FT596 clinical data presented thus far reflect activity following a single- dose of FT596. We believe our iPSC product platform provides a unique opportunity to maximize the therapeutic potential of cell-based cancer immunotherapies, and we are actively exploring additional levers of opportunity for FT596. First, we are continuing dose escalation to increase the cell dose in a single- dose treatment cycle. Second, we are introducing a multi-dose treatment cycle with FT596 administered on day 1 and day 15 of the treatment cycle. Third, similar to the paradigm established with FT516, we are assessing administration of a second treatment cycle. Let's discuss this second treatment cycle a bit more. Under the current protocol for FT596, a second single-dose treatment cycle may be administered to a patient with FDA consent. All requests for retreatment that we submitted were approved by the FDA. As of the data cutoff date, eight patients in dose cohorts 2 and 3 have been retreated with a second single-dose treatment cycle. The clinical course of patients receiving this second single-dose cycle notable for the following. First, the second FT596 cycle was well tolerated in that there were no events of any grade of CRS, ICANS, or GVHD. Second, the clinical activity of the first FT596 was maintained. Four patients with a complete response after cycle 1 were retreated and maintained complete response after cycle 2. Response assessments for the other four patients were pending as of the data cutoff date. Based on the data submitted to the FDA to date, the FDA has recommended that Fate amend the clinical protocol to allow retreatment with a second FT596 treatment cycle without requiring FDA consent. Now I will turn it over to Sarah to review key translational findings from our FT516 and FT596 studies. Thank you, Wayne. I'd like to briefly discuss some key data and observations from our translational investigations. First, I will address the potential of host immune cell rejection of FT516 and FT596. The mechanisms by which allogeneic cell products may be rejected are not fully understood, and approaches to overcome rejection are not well established in the clinic for allogeneic cell products. That said, the importance of lympho-conditioning is well recognized across the field of cell therapy, including for the success of autologous CAR T therapy. In addition to inducing homeostatic cytokines, lympho-conditioning depletes potentially alloreactive host T and NK cells, creating a window of opportunity for allogeneic cell products to induce durable antitumor activity. In our clinical studies, we are closely investigating key determinants that define this window of opportunity for our cell products. As part of our investigations, we use a modified mixed lymphocyte reaction, or MLR assay, as shown in the cartoon on the left, to assess the reactivity of patient lymphocytes against product cells at various time points during the course of FT516 or FT596 treatment. Reactivity of patient lymphocytes is measured based on interferon-gamma production by ELISpot and is compared against an alloreactive control that has been established using peripheral blood mononuclear cells primed to recognize and kill our product cells. Shown on the right are the median and interquartile range of interferon-gamma-producing patient lymphocytes sampled at the end of cycle 1 or cycle 2 of FT516 and FT596 treatment after co-culture with our product cells. All groups demonstrated less than 10 positive counts, comparable to that of the negative control and significantly lower than the alloreactive control, which gave greater than 300 positive counts. Of note, we can also correlate the interferon-gamma score to our companion in vitro cytotoxicity functional assay, where we have determined that the measurable cellular cytotoxicity is not observed until well above the range of 100 positive counts. Thus, for both FT516 and FT596, our data demonstrate minimal product-specific recognition after 2 cycles of treatment, and there is no evidence of functional cytotoxicity by patient lymphocytes against the cell products. Similar to our previous observations, we also looked for and were unable to detect the development of antibodies specific to the cell products. Our inability to detect host immune cell rejection of FT516 and FT596 is consistent with the peripheral blood PK data shown here for FT516. PK is assessed at multiple time points after infusion using a digital droplet PCR assay that measures the hnCD16 transgene. Shown here are the hnCD16 transgene copies detected in patients at cell doses of 90 million in green and 300 million in red. The dots represent individual patients with the mean of each dose cohort represented by the bar. As shown, FT516 is detected after each of the three weekly infusions, supporting our findings that FT516 is not being rejected. For each dose, the FT516 copy number decreases over a seven-day period, which is not unexpected as NK cells have a short half-life. Notably, the second and third doses of FT516 do peak at lower amplitudes compared to the first dose, and this may be due to numerous factors evolving during the treatment cycle, including a decrease in FT516 survival resulting from a decrease in cytokine availability, decrease in antigen-driven FT516 proliferation resulting from a decrease in tumor burden, and/or differential trafficking of FT516 out of the blood and into other tissues based on homing cues. We're also keenly interested in differences that we might observe between FT516 and FT596, which again incorporates the CD19 CAR construct as well as the IL-15 receptor fusion for cytokine support. Here, we are comparing the peripheral blood PK of the first dose of FT516 in red with that of a single- dose of FT596 in blue. Again, individual patients are represented by dots, and the median values are shown as bars. Remember, FT516 is administered with IL-2, while FT596 is administered without any exogenous cytokine support. We find that a single- dose of FT596, administered without IL-2, persists at a higher frequency and for a longer duration compared to the first dose of FT516. We believe that this differential profile of FT596 reflects the ability of its engineered IL-15 receptor fusion modality to provide autonomy from homeostatic cytokines induced by the lympho-conditioning regimen. This is exciting, as the experimental conditions are identical, the same patient eligibility, the same Cy/Flu regimen, the same cell dose. This certainly validates the potential to effectively administer FT596 without the requirement for exogenous cytokine support. That said, it is important to emphasize that while these peripheral blood PK data demonstrate differences between FT516 and FT596, we have not seen a correlation between peripheral blood PK and response. It is important to recognize that NK cells are not T cells, and surrogates of activity for the CAR T- cell field may not apply to NK cells. More work is ongoing here to determine the best surrogates to correlate with response. Lastly, I'd like to share a case study from a patient treated on the monotherapy arm of the FT596 study, which demonstrates the ability of the CD19-directed CAR to overcome CD20 antigen escape. This 78-year-old patient had received four prior therapies, including three CD20-targeted regimens. Her baseline tumor biopsy demonstrated high expression of CD19 and complete loss of CD20. She was treated with a single- dose of FT596 at 90 million cells as monotherapy. Peripheral blood samples taken throughout her treatment course demonstrate the kinetics of clearance of the CD19-positive malignant population and recovery of the phenotypically normal B cell population. At day - 5, prior to treatment, both normal CD19-positive, CD20-positive B cells and malignant CD19-positive, CD20-negative lymphoma cells are present. At day 4, immediately after the FT596 dosing, the normal cells have been ablated while the malignant cells show resistance to the Cy/Flu lympho-conditioning. By day 29, the normal B cell population is recovering while the CD20-negative lymphoma cell population continues to decrease. After one cycle, she achieved a complete response with complete resolution of all metabolically active disease, a 92% reduction in tumor size, and the clearance of the lymphoma from her bone marrow that had been present at baseline. By day 104, without the benefit of a second FT596 treatment cycle and with no further intervening therapy, a robust recovery of normal B cell population was observed with complete elimination of the malignant cells. This example highlights the value of multi-antigen targeting to overcome antigen escape, a common mechanism of resistance to standard CD19 or CD20-targeted therapy, and to drive a durable, complete response. At this point, I will turn it back to Scott for some final comments. Thanks, Sarah. Our mission at Fate Therapeutics is about changing the game in cell therapy. While cell therapies hold extraordinary potential, the business of making and delivering a cell therapy is massively complex, very often personalized, and far too limited with respect to patient reach. Our vision is to develop and deliver cell therapies in a manner similar to monoclonal antibody therapy. A renewable cell line is used for manufacture. Product is mass-produced in a cost-effective manner. The product is conveniently administered in a thaw-and-infuse manner, and many patients have access to and receive the product with the urgency needed to treat cancer. We believe our iPSC product platform is uniquely delivering on this promise. While we believe our iPSC product platform confers unparalleled advantages compared to patient and donor-derived cell therapy approaches, our focus is on bringing best-in-class cell products to patients. To that end, I want to summarize a couple key observations from today. With respect to product efficacy, early clinical data from our FT516 and FT596 programs in difficult-to-treat patients demonstrate compelling response rates, and the maturing durability of response data from our FT516 program indicate that the clinical benefit can be lasting. We have shown that our proprietary hnCD16 Fc receptor can uniquely synergize with and enhance the mechanism of action of tumor-targeted antibodies, and that both FT516 and FT596 can be effectively deployed in combination with CD20-targeted monoclonal antibody therapy to enhance patient outcomes. The clinical benefit mediated by our hnCD16 Fc receptor has been shown to be deep and early data suggests the potential for significant durability of response. Additionally, we have demonstrated the activity of our novel CAR construct incorporated into FT596 and its potential to drive high response rates with a single-dose treatment schedule in heavily pretreated patients. Together, the integration of these two elements into FT596 enable multi-antigen targeting and a potential best-in-class therapeutic profile, with the ability to attack tumors through multiple mechanisms of action to effectively address tumor heterogeneity and to uniquely overcome antigen escape. With respect to product delivery, we have shown that FT516 and FT596 are available on demand at the time of patient need. We have demonstrated the ability to serve patients in the outpatient setting with over 85% of FT516 doses administered outpatient. We have also demonstrated the ability to deliver multiple doses without eliciting host T or B-cell-mediated rejection, a treatment paradigm that may drive deeper and more durable responses. Finally, with respect to safety and tolerability, we have continued to show that our iPSC-derived NK cell product candidates are well-tolerated and have a profile that is differentiated. We believe this favorable profile will facilitate combination with other therapies, including those used as standard of care in earlier lines, and will allow patient reach into the community setting. Where do we go from here? With respect to FT516, we're currently planning to initiate multiple dose expansion cohorts to further assess its efficacy. These cohorts include third-line diffuse large B-cell lymphoma and third-line follicular lymphoma, both in patients that are naive to autologous CD19 CAR T-cell therapy. Additionally, since we have observed complete responses in two of four patients in dose cohorts 2 and 3, whose disease progressed following autologous CD19 CAR T-cell therapy, we plan to initiate a dose expansion cohort in patients with aggressive B-cell lymphomas that have been previously treated with autologous CD19 CAR T-cell therapy. We believe this dose expansion cohort in particular addresses a growing market segment with a significant unmet need and may offer a potential fast-to-market development path. Finally, since FT516 may be administered in the outpatient setting given its favorable safety profile, we plan to initiate a dose expansion cohort of FT516 in combination with bendamustine and rituximab, and without Cy/Flu chemotherapy conditioning to explore its use with standard of care, CD20-targeted regimens in earlier-line therapy. In these dose expansion cohorts, we intend to include sites that serve patients in a community setting. With respect to FT596, we are currently enrolling the single-dose treatment schedule at 900 million cells in both the monotherapy and combination arms. We are initiating enrollment in the two-dose treatment schedule beginning at 300 million cells in both the monotherapy and combination arms, and expect to dose escalate the two-dose treatment schedule to 900 million cells. Based on observed safety and efficacy, we expect to select either the single- dose or two-dose treatment schedule for conduct of dose expansion. As a reminder, based on the FDA's recommendation to amend the FT596 clinical protocol, retreatment with a second FT596 treatment cycle without requiring FDA consent will now be permitted. Finally, we are poised to expand clinical investigation of our off-the-shelf multiplex engineered iPSC-derived NK cell franchise to multiple myeloma. Similar to our approach in lymphoma, we are beginning clinical investigation by leveraging our hnCD16 receptor, combining FT538 with the CD38-targeted monoclonal antibody daratumumab to maximize ADCC. We're also advancing FT576, our off-the-shelf iPSC-derived CAR NK cell product candidate designed to target multiple antigens through its hnCD16 receptor and its high avidity BCMA-targeted CAR. We are poised to begin clinical study of both FT538 and FT576 in multiple myeloma and look forward to bringing patients these potentially best-in-class therapies. Thank you for your time today. I would now like to open the call up to any questions, and Ed will moderate those. Great. Thank you, Scott. We've had a number of questions come in during the presentation, but as a reminder, you can ask a question by utilizing the questions and answers functionality within the webcast presentation. First question is about dose response, specifically related to FT596. There's an observation that there's clearly an effect from 30 million-90 million cells, but an observation of this leveling off potentially from 90 million-300 million cells. So have we reached an optimal dose at 90 million? Or just general comments about dose response for FT596. Sure. Wayne, do you want to comment on that? I think it's very clear that with respect to FT596, there's clearer evidence of dose dependency just given by the fact that at 30 million cells, we see only one out of six responses. Certainly as we get to the 300 million cell dose level, we see six out of seven. Whether or not the trend of that dose response is maintained, I think it's just going to require more data because I think that, as everyone can appreciate, these patients are highly heterogeneous. There may be other factors that contribute to that dose response. As we further optimize our dose and schedule, I think we'll definitely have that opportunity to determine what that dose response relationship is, not only with respect to the number of cells per dose Cells that are delivered over multiple doses. Thanks, Wayne. Second question, multipart question. We'll take this in pieces. Talking about FT516 and the durability of complete responses, what can we say at this point versus allogeneic CAR T? I'll take that. I think it's too early to know ultimately what the long-term durability of FT516 is and how that compares to CAR T-cell therapy. I think we're encouraged to date that the three-month durability of response, I think, is similar to CAR T-cell therapy. I think we noted it was 73% OR and 55% CR, which I think is in line with even autologous CAR T-cell therapy. I think we're very encouraged by the durability that we're seeing as we continue to follow these patients. Four of the 11 patients remain in CR. Several of those, I think we alluded to, were refractory to prior therapy. In fact, one of those was previously treated with CAR T-cell therapy and continues in CR. A follow-on question about bringing FT596 into the equation, moving to multiple doses per month, the potential for higher CR rates, thus a potential benefit in terms of durability. Any thoughts on FT596 versus FT516? Yeah. I think FT596 we continue to believe is a best-in-class product candidate, absolutely. I do believe that patients can be aided by additional therapy. We've certainly reported that in the past for FT516, and we have reported that for FT596. I think it's important to note that as we have retreated patients, we've continued to see maintenance of response and in some cases, deepening of response. I do think there's a benefit to continue to add a second cycle, as long as it's well-tolerated, and that that second cycle can drive deeper and more durable responses. Thanks, Scott. The next question, again, FT516 and FT596. Have we learned anything about the second or third dose in a cycle of FT516 versus what we're moving to with FT596 in terms of going from a one dose to a multi-dose paradigm, and what we expect the read-through might be for FT596? I'll start, and then I'll allow Sarah to jump in. Look, I think what we have seen, and we've seen with the PK data, and again, the blood may be a poor proxy ultimately for measuring NK cells. I think we have seen that certainly with FT516, we've been able to safely deliver three different doses, that those three doses are detected. We've seen that actually the second cycle with FT516 can add patient benefit. We've seen certainly deepening of responses from the first cycle to the second cycle with FT516. With respect to FT596, I think the data that Sarah presented has clearly shown that the first dose of FT596 is at least, again, using the blood as the proxy, which may be a poor proxy, but is certainly outperforming FT516 with respect to its presence in the blood and its persistence. I do think as we look at, for instance, FT516 being administered in a three-dose treatment schedule, we are confident based on what we're seeing with FT596, including the response rates, as well as the PK, that a two-dose schedule for FT596 in a cycle is the right schedule. I don't know, Sarah, if you have anything to add to that. No, I agree with how you characterized it, and I guess I would just add that clearly this is not an apples to apples experimental design to understand multi-dosing versus single dosing. The protocol amendments that Wayne spoke of will give us more opportunity to look at how FT596 behaves in a multiple dose per cycle schedule. Thank you, Sarah. Next question is around durability for FT516, and how do we think about this in the context of approved CD19 autologous CAR T-cell therapies, and specifically this six-month rule as it relates to CR rates that relevant in the context of NK cells and FT516 specifically? Yeah. I think, look, the reality is there are multiple autologous CAR T-cell therapies that are approved. I think, if I'm going to get this right, and Ed, you're an expert in this, so you can correct me, but the six-month CR rate for the autologous CAR T-cell therapies ranges anywhere between, say, 30%-35%, something in that range with respect to the six-month CR rate. If I look at our data today, we're right in that range with FT516. Four of 11 patients remain in CR, anywhere between 4.6 out to 9.5 months. A fifth patient is in continuing PR. I feel really good about where we are with respect to FT516, which keep in mind, doesn't have a CAR, and its ability to synergize with Rituxan and drive responses. I think one of the things we're trying to accomplish with FT516 and we're excited about is the potential to look at its ability to be used downline of CAR T-cell therapy, where we've clearly been able to show that patients that have progressed after CAR T-cell therapy are able to respond, and they are responding with degrees of durability, which is exciting to see. In addition, going to the other end of the patient spectrum, I do think we have a differentiated safety profile, and clearly we've administered, I think Wayne mentioned, about 85% of the doses in the outpatient setting. I think we have the ability to move to earlier lines of therapy, essentially become an add-on to a rituximab regimen that is used standard of care in earlier line. I think CAR T-cell therapy will have a very difficult time moving into that outpatient paradigm. Thanks, Scott. The only thing I would add is those CR rates and response rates, typically in autologous CAR T are done on a modified intent-to-treat population, where ours is obviously an ITT population. The next question, straightforward one related to FT596, and do we have any thoughts on the value of potentially adding IL-2 to the treatment regimen for FT596? At this point in time, we don't plan on adding IL-2 to the treatment regimen. We're pretty excited about what we're seeing with the IL-15 receptor fusion that is engineered into the product candidate. Clearly we are seeing, at least again using peripheral blood as a proxy, we're seeing FT596 outperform, if you will, FT516, which is aided by IL-2, but does not have the benefit of the IL-15 receptor fusion. Thank you, Scott. Next question related to FT596 and about repeat or second-cycle dosing. For all the patients that received a second cycle of FT596, were those all patients who had an initial response for the first cycle? The second part of the question is, do we have any data suggesting treating someone in the first cycle who did not respond, and whether or not there's a benefit of that subsequent FT596 cycle? I believe Wayne can jump in, but I believe all the patients that were retreated with FT596 had a response at the end of their first cycle, and that response was either maintained or deepened with the second cycle. We do not yet, to my knowledge, and Wayne jump in, we don't have any experience yet with treating a patient that has not responded following the first cycle. Wayne, you may confirm that. Yeah. That's indeed true. As Scott mentioned, all patients who were retreated had at least a partial response after the first cycle. Also, as Scott mentioned, we do have cases where we have evidence of a deepening response after the second cycle of treatment. Then in patients who achieved a complete response after the first cycle, as we've stated in the presentation, those patients were able to maintain that complete response. Thanks, Wayne. A number of questions around the expectations for ASH as it relates to the durability update we should expect for both FT516 and FT596. Yes. I think we do plan on providing additional updates to both the FT516 and FT596 programs at ASH. I expect we'll get our first look at durability with respect to FT596, certainly in the single-dose treatment paradigm. Great. We have a number of questions about next steps. I think we addressed some of this in the presentation. Questions around have we determined what the recommended phase II dose is, as the first part of the question. There's a couple of follow-ups as well. I don't think we've determined yet what the recommended phase II dose is. I think with respect to both FT516 and FT596, we're at the top end of what we think is dose escalation at this point, at 900 million cells as the dose level. We'll generate that data set, look at the data, and then obviously proceed with what we think is the right dose for the expansion. Okay. Then for FT516 specifically, any more details around the plans for engaging with regulatory authorities, and are we able to give any loose timelines with respect to potential BLA filings? What would be earliest date for FT516? I think it's too early to make a comment on BLA filings, but I will comment on regulatory engagement. As we complete dose escalation for FT516, which should wrap up in the next couple of weeks, we do plan on submitting an RMAT application to the FDA to begin to engage in a more formal way with respect to a pivotal path for FT516. I think our initial sense is that a potential fast path to market is treating patients that have progressed or failed autologous CAR T-cell therapy, where we've certainly seen responses with both FT516 as well as FT596. Thanks, Scott. There's a number of questions about an interest in learning more about the expansion as it relates to bendamustine Rituxan combination. Any other additional comments around design or timing for that expansion or plans beyond that would be useful. Sure. Wayne, do you want to comment on that? Sure. Regarding rituximab and bendamustine, that is a combination that will be initiated very soon with FT516. As was mentioned in the presentation, the concept around combining FT516 with something like R-Benda takes advantage of R-Benda's properties, both with respect to the anti-lymphoma activity as well as the ability of agents such as bendamustine to act as a conditioning agent to support FT516 pharmacokinetics. That piece of FT516 is already included in the most recent protocol amendment, and we expect to enroll patients testing that combination very soon. Okay. Thank you, Wayne. Question relates to FT596. We've mentioned multi-antigen targeting on a number of occasions. Question specifically is around, is this referring to CD19 and CD20 only, or are there other antigens that we're considering as well? Certainly, I think with the Fc receptor, this hnCD16 Fc receptor, we feel there's the ability to engage multiple different monoclonal antibodies, for instance, and target a variety of antigens where there is a monoclonal antibody that is available for targeting. For instance, we are leveraging that receptor clearly in combination with rituximab. We will leverage that receptor in combination with obinutuzumab, both in the lymphoma setting. We're leveraging the CD16 receptor in combination, for instance, with daratumumab, both in AML and lymphoma. Certainly, as we think about solid tumors as well, we look forward to leveraging the hnCD16 receptor in combination with monoclonal antibodies that are used thoroughly and often in treating solid tumors. Thanks, Scott. Question generally about chemotherapy induction and the necessity for this for our NK cells, including FT596, that has IL-15 receptor fusion. Yeah. Sarah can comment on that. I think it's one of the reasons we're interested in combining with R- bendamustine, and I'll pass hand it over to Sarah. Across the field, lympho-conditioning, traditionally with Cy/Flu, is utilized. As I mentioned, understanding the specific elements in terms of inducing IL-15 and other homeostatic cytokines versus clearing space versus eliminating potentially alloreactive cells all play a role. It's our hope to dissect out for our products in specific which of these elements are necessary. For example, the data with FT596 demonstrates that perhaps the need to induce IL-15 from the patient is not there if we've engineered that element into the cell. We're actively investigating opportunities to use less intense conditioning, specifically with the bendamustine arm that will be opening soon that Wayne mentioned, and other paths to look what is the minimal necessary lympho-conditioning that we need to add to allow that window of opportunity for the cells to proliferate and achieve the anti-tumor effect sufficient for durability. Thank you, Sarah. Next question about patients previously exposed to autologous CD19 CAR T therapy. Do you have any reason to believe that FT596 or FT516 in combination with rituximab would reactivate or reinvigorate CD19 CAR T- cell therapy? Have we looked at this in any of the responses that we've seen in advanced refractory patients? I'll take that. It's an intriguing question. We're very interested to understand if we can resuscitate either autologous CAR T- cells or just plain autologous T cells in the patient. We're doing extensive immune profiling to understand the characteristics of the reconstituting T cell compartment to look for interactions between our product and the patient T cells. I'll add it's slightly difficult to evaluate other parts to pick out the CAR T- cells in patients who've undergone prior therapy with the approved products, but it's something that we're actively looking at. I would just also add that in those patients who've received prior autologous CD19 CAR T therapy and were treated with either FT516 or FT596, as we kind of alluded to in the presentation, we don't see anything, at least from a safety perspective, that suggests a profile of either cytokine release syndrome or ICANS that strongly indicates a pattern of reactivation of CAR T- cells, knowing that, at least anecdotally, that some of the patients who received prior CAR T did have some level of CRS when they received CAR T that was not replicated with the administration of our iNK cell product. Okay. Thanks, Sarah. Thanks, Wayne. Question relates to FT596 and then moving towards multiple doses and potentially up to two cycles. Is this more in the context of driving greater durability? Do we have a clear understanding, looking at immune response, what that right frequency of dose and schedule are for FT596 to drive durability similar to CAR T response? I think it's too early for us to answer that question. I think clearly with FT516, we've been able to demonstrate we can safely administer three doses in two cycles. I think with the PK data and the response rates that we're already seeing with FT596, we certainly believe that we can drive significant responses off a single- dose and a single cycle. We strive to deliver the best product candidate to the patient. Our platform allows for dosing flexibility, and we believe that that's worth exploring here at higher doses as part of dose escalation before we move into an expansion. Thanks, Scott. The next question I think we've addressed at some level in the presentation, but as it relates to FT596 and responses of monotherapy patients versus the combination. Is it more difficult to treat set of patients in the combination arm, or explain the lower response rates observed in that combination with Rituximab? Yeah, I think it's hard to make generalization on, relatively speaking, small numbers of patients. Yeah, I think as Wayne Chu alluded to in the presentation, I think the patients in the combination arm were more difficult to treat. A higher percentage of them had had CAR T-cell therapy previously, had had refractory disease, had greater tumor burden. I would note the CR rate was, in fact, higher in the combination arm. Thanks, Scott. The next question, also related to FT596. Maybe, Wayne, this is a question for you if we've cut the data. We're looking for response rate and CR rates in aggressive versus indolent lymphoma histologies for FT596. Yeah. For FT596, based on the information that we presented with the individual patient's data and then presentation, just by the hand count. For diffuse large B-cell lymphoma, and I would actually include the one case of Grade 3B follicular lymphoma in that category, because for all in terms of clinical outcomes, they are similar. There were a total of seven patients with DLBCL and the one case that's Grade 3B follicular lymphoma. Four of those seven had an objective response, three of which were complete responses. For follicular lymphoma, which is Grade 1 to 3A follicular lymphoma, there were a total of four patients. Three of them had a response, and all three of them were complete responders. Just for completeness sake, the remaining three patients had other types of lymphomas. All three had responses, and one of them was a complete response. I should point out that these numbers, a total N of 14, reflect those patients treated at a cell dose level of 90 million FT596 cells or higher. Thank you. Next question, again, about FT596. Translationally, do we look for cell expansion and durability, either PCR or flow cytometry, to understand the expansion and durability of FT596 cells post-infusion? This is more of a question about the functionality and validating the functionality of the IL-15 receptor fusion. The data I shared comparing FT516 and FT596, you can see the PK profile and kinetics of the FT596 product after infusion. We, when possible, collect the cells from the peripheral blood if they're there in sufficient numbers to evaluate the function of the product cells over time in vivo after being exposed to tumor. I don't have specific details that I can share with you now about changes in the function compared to infusion and after in vivo exposure, but that's something that we're characterizing closely. Thank you. Follow-on question, just generally, I guess FT516 or FT596, about evading endogenous immune clearance. Do you have any sort of engineered cells, anything about stealth of our capability there, whether they're required and whether or not they're engineered, thought about for a FT516 or FT596? Can I just make one comment? That the data that we showed today, so far for FT516 and FT596 at the doses infused, we're not seeing evidence that there's immediate host rejection. Today it's not a problem that we're seeing. However, in the future it could develop. I'll let Bob comment. Sure. No, I agree with Sarah completely. Right now we're seeing for the first two months no recognition. If we were to see that, I think we have multiple programs that we'll be updating you at ASH on unique strategies that I think are best in class, and look forward to sharing that with you guys then. Thanks, Bob. Question on FT516, the lower Cmax, the three-dose schedule of 516 plus rituximab, are we considering any modifications to the schedule as we think about expansion cohorts or studies beyond phase I development? No, I think at this point, we're really pleased with what we're seeing with respect to FT516. We're seeing clearly that three doses can be well-tolerated in the first cycle. We've seen evidence that in certain patients, that the second cycle is clearly adding to a deepening of response. At this point in time, based on the response rates that we're seeing and the durability of response, including downline of CAR T-cell therapy, I think we're very comfortable in filing our RMAT submission and engaging with the FDA to plan for a pivotal study. Again, most likely with FT516, will be focused on patients that are downline of CAR T-cell therapy, or in patients that we plan to treat earlier line with a standard of care rituximab regimen. Thank you, Scott. Wayne, maybe back to you. A question around FT596. I think we addressed this in the presentation, but there, talk about the wide spectrum of histologies within our phase I study. How do these patients compare to a more traditional third-line DLBCL population in terms of aggressiveness of disease? As it relates to a late-line relapsed refractory population with aggressive disease, I would say that based on the characteristics that we presented with respect to prior therapies, degree of refractoriness, the advanced stage of disease and overall tumor burden, I think at some level, it is very comparable to what one would expect in this particular patient population, particularly with respect to the number of prior therapies. I think that the advanced stage and the significant tumor burden that we see in these patients are just reflective of the fact that for patients who don't get cured with initial treatment options are extremely limited, and despite multiple efforts, a patient's underlying aggressive lymphoma continues to grow. Okay. Thank you, Wayne. In terms of FT516 or FT596, do we see a correlation with Cmax in tumor burden programs? Yeah. We've looked for multiple things that could predict Cmax or response or PK, and we have not been able to correlate tumor burden or tumor histology with the PK profile at this point. Maybe one or two more questions. Great. The next question talks a little about from the regulatory perspective in patients with prior CAR T, do we have a sense of what the bar would be in terms of clinical benefit and durability specifically? I think it's too early to comment on that. Next question about product-specific or lack of product-specific anti-HLA antibodies. Is the same after issuing subsequent cycles of FT516 or FT596? Yeah, that's a good question. I touched on that too briefly. We look for the development of anti-product HLA class one and class two antibodies, and we haven't seen, in the patients on FT516 or FT596, any development of any anti-product antibodies after cycle 1 or cycle 2 to date. Thanks, Sarah. Last question? Yep. Last question. With respect to FT596 and where we are in dose escalation at 900 million cells, just clarification on where we expect to be at ASH in December. All right. ASH in December, I think we will continue to backfill in the single-dose cohort. We will continue to backfill at the 300 million cell dose. We will continue to escalate now at 900 million cells, which we will also likely backfill. We are probably between now and ASH, we're looking to backfill 300, complete 900 with up to six patients. In addition now, begin to treat patients at 300 million cells with the two-dose treatment schedule. I think we'll have a pretty fulsome update with FT596 at ASH, including on durability of the responses that we're seeing. Great. Scott, back to you. Thank you. Thank you, and thank you everyone for participating in today's call. Be well.