Thank you for holding. Good morning, and welcome to the Passage Bio conference call. At this time, all participants are in a listen-only mode. Following the formal remarks, we will open up the call for your questions. Please be advised that this call is being recorded at the company's request. At this time, I'd like to turn it over to Stuart Henderson, Vice President of Corporate Development and Investor Relations. Stuart, please proceed. Thank you, operator. Today, we will review interim results from the global upliFTD Phase 1/2 clinical trial of PBFT02 in frontotemporal dementia. Please refer to the press release issued recently and the slides that we will be using on today's call on the Investors and News section of the Passage Bio website. Before we begin, I'd like to remind you that our presentation will contain forward-looking statements based on our current expectations and beliefs of future events as of today. These statements are subject to a number of risks and uncertainties, including those risk factors from our latest 10-Q, that could cause actual results to differ materially and adversely from those presented. It is now my pleasure to turn the call over to CEO, Dr. Will Chou. Will? Thank you, Stuart. I'm excited to share the first clinical data from our ongoing upliFTD Phase 1/2 clinical trial of PBFT02 in patients with frontotemporal dementia caused by a granulin gene mutation. I'll begin today's discussion by providing an executive summary, and then Dr. Mark Forman, our Chief Medical Officer, will review the interim findings in more detail. I will then close the discussion by reviewing additional therapeutic areas we plan to explore with PBFT02. Turning to slide 5, frontotemporal dementia, or FTD, is a devastating adult neurodegenerative disease for which there are no disease-modifying therapies currently approved. Our upliFTD study is focused on patients with a granulin gene mutation, resulting in haploinsufficiency and progranulin deficiency. Granulin gene mutations are estimated to account for up to 10% of all FTD cases, affecting up to 18,000 patients in the US and Europe. FTD-GRN is a rapidly progressing form of FTD, characterized by loss of speech, expression, severe behavioral changes, and immobility. On slide 6, we describe our product candidate, PBFT02. PBFT02 is a gene therapy that utilizes a proprietary AAV1 construct to deliver a functional copy of the granulin gene, which encodes progranulin. Our approach offers the potential therapeutic benefit of a one-time treatment and delivers the vector directly to the CSF via a single injection to the cisterna magna. In preclinical studies, PBFT02 achieves supraphysiologic levels of CSF progranulin. Today, we are excited to report that initial data from cohort 1 in this first-in-human study shows that our initial dose level of PBFT02 has also achieved supraphysiologic levels of CSF progranulin. Turning next to slide 7, upliFTD is our Phase 1/2 first-in-human study for PBFT02, and the key objectives are focused on establishing the safety, tolerability, pharmacokinetic, and pharmacodynamic effects of our investigational gene therapy. In establishing the safety profile of PBFT02, in addition to assessing potential adverse events and toxicities, the goal in any first-in-human AAV study is determining the correct level of immunosuppression to safely and effectively administer the product. Another crucial goal of the study is to identify the optimal dose of PBFT02 that achieves the most significant therapeutic effect in FTD-GRN patients. Finally, we hope to obtain a comprehensive understanding of the benefits of PBFT02 treatment across symptomatic FTD-GRN patients. This includes assessing the effects of PBFT02 on a variety of target engagement and pharmacodynamic biomarkers, as well as the rate of disease progression as measured by the Clinical Dementia Rating scale. On slide eight, we are excited to summarize interim findings from the first three patients in the study. Beginning with safety, our study protocol started with a low level of oral steroids only for immunosuppression. At this level of steroids, patient one experienced two SAEs consistent with an immune response. The study protocol was then revised to increase the steroid regimen for subsequent patients enrolled in the study. In contrast, patients two and three, who received a higher level of steroid immunosuppression, did not experience SAEs. Only mild to moderate treatment-emerging AEs were reported in these patients. In all three patients, there was no evidence of dorsal root ganglion toxicity as measured by nerve conduction studies, and there were no complications related to the intra-cisterna magna administration. Turning next to efficacy and target engagement. Based on our preclinical data, one of the core differentiating features of our program was that PBFT02 had the potential to achieve supraphysiologic levels of CSF progranulin. We are thrilled to report that the first three treated patients indeed all achieved supraphysiologic CSF progranulin levels at day 30 after receiving only the initial dose level of PBFT02. These patients achieved a 4- to 7-fold increase in CSF progranulin over baseline, which outperforms levels we would have expected based on preclinical studies. Importantly, supraphysiologic CSF progranulin levels were sustained at 6 months post-treatment in the one patient with this length of follow-up. Overall, we are very excited by what we've learned to date about the potential of this product, and look forward to continuing to share results over the coming quarters. With that, I'd like now to turn the call over to Mark. Thanks, Will. Moving to slide 9, I'll begin first by reviewing the role of progranulin and the supporting data for our program, and then detail the findings from this initial analysis. Turning now to slide 10. Progranulin is a secreted glycoprotein derived from the granulin gene that is mainly expressed by neurons and microglia, and plays a critical role in maintaining cellular homeostasis in the central nervous system, or CNS. It is well understood that decreased progranulin levels in patients with FTD-GRN lead to neuronal dysfunction, pathological changes, including TDP-43 pathology, synaptic dysfunction, and inflammation. These changes, in turn, affect neuronal health in various regions of the brain, ultimately leading to neurodegeneration. Next, on slide 11, we review some of the supporting preclinical data for PBFT02. This slide shows the result from vector exploration studies in non-human primates. On the left, you can see CSF progranulin levels over time for AAV5 in red, AAVhu68, which is a proprietary capsid similar to AAV9 in blue, and AAV1 in green. As you can see, AAV1 outperformed the other vectors in terms of levels of CSF progranulin achieved, and was able to drive levels substantially higher than the normal reference range for healthy adult controls of about 3-8 ng/ml, depicted by the gray shaded zone. This finding was central to the selection of AAV1 for our PBFT02 program. On the right, you can see plasma progranulin levels over time for the same vectors tested. Importantly, plasma levels remained in the normal range in the periphery, despite supraphysiologic levels centrally, suggesting that the effects of ICM administration of vector are relatively confined to the CNS. Moving to slide 12. As discussed earlier, progranulin plays a key role in cellular function within the CNS, particularly within neurons and microglia. Importantly, all the biological effects require progranulin to function intracellularly. Progranulin is secreted extracellularly and then taken into target cells via several receptors. Once inside the cell, progranulin affects multiple intracellular pathways, including lysosomal function, cell signaling and proliferation, and inflammation. By substantially raising levels of progranulin extracellularly, we are increasing the amount of protein available to receptors to exert the appropriate downstream intracellular effect. We would expect these higher levels of intracellular progranulin to translate into improved cellular functions. The rationale for the importance of achieving supraphysiologic levels of CSF progranulin is further supported by preclinical findings detailed on slide 13. The left panel details lipofuscin levels from a murine FTD model. Increased levels of lipofuscin are associated with lysosomal dysfunction, which is correlated with the disease pathology of FTD-GRN. In this study, granulin knockout mice are shown to have elevated lipofuscin levels at baseline, which is reduced at all dose levels of PBFT02 tested, suggesting correction of the underlying mechanism of the disease. Next, on the right panel, we show microgliosis findings from the same murine FTD model. Microgliosis is an inflammatory response to pathogenic insults in the CNS and is measured by staining for CD68, a marker of activated microglia. Granulin knockout mice have elevated microgliosis at baseline, which is reduced by administering PBFT02. However, the reduction is most pronounced at the highest dose of PBFT02, the only dose that achieves supraphysiologic progranulin levels in mice. This suggests that correction of certain cellular functions may only be achieved at supraphysiologic levels of CSF progranulin. Moving to slide 14. This slide details results from a dose-ranging study of PBFT02 in non-human primates. In this study, PBFT02 was administered via ICM injection to non-human primates to deliver human progranulin. The data displayed showed the levels of human progranulin achieved at 14 days post-dosing. Keeping in mind that the estimated level from healthy adults is approximately 3-8 nanograms per ml, you can see that the low dose, which corresponds to dose 1 in our upliFTD trial, achieved levels towards the low range of normal.... The next two dose levels then achieved higher levels of human progranulin in CSF, with the highest dose achieving supraphysiologic levels at day 14. It's worth noting, however, that non-human primates develop an immune response to human progranulin, which may underestimate the actual level that is achieved in humans following ICM administration of PBFT02. Let's now review our ongoing upliFTD clinical trial on slide 15. The upliFTD trial is a global, multicenter, open label dose escalation study evaluating two dose levels of PBFT02 with an optional third dose. upliFTD is a two-year study with rollover into a long-term follow-up study. The primary endpoint of the study is to evaluate the safety and tolerability of PBFT02. Secondary endpoints include various biomarkers measuring target engagement and pharmacodynamic effects, as well as clinical outcomes. In addition, we are evaluating several exploratory biomarkers associated with lysosomal dysfunction. Today's results will focus on target engagement, specifically CSF and plasma progranulin levels in the first three treated patients from cohort one. Other pharmacodynamic biomarkers and clinical outcomes require longer follow-up to determine treatment effect, so we will not be sharing this data today. Slide 16 describes the inclusion criteria for the study. We were enrolling symptomatic FTD-GRN patients who have a confirmed clinical diagnosis and pathogenic granulin mutation. Patients enrolled must be between 35-75 years of age, living in the community, and have a reliable informant or caregiver. Next, we have provided baseline characteristics of the first 3 patients treated on slide 17. The initial patient enrolled in the study were between 51-60 years of age, with low levels of CSF progranulin at baseline, as expected. The Clinical Dementia Rating scale, or CDR, used in the study, is modified for patients with frontotemporal dementia. The sum of boxes score has a range from 0-24, with higher scores indicating greater impairment. Based on their CDR scores at baseline, these patients manifested mild to moderate impairment. Slide 18 is a schematic of the spectrum of immunosuppression regimens that may be used in AAV gene therapy clinical studies. Moving from left to right, there's a range of immunosuppression increasing from steroids alone to steroids plus inhibitors of T cell and/or B cell function. The initial upliFTD protocol started with a relatively low level of steroid immunosuppression, and patient one received only 60 milligrams oral prednisone daily for 60 days. With this level of immunosuppression, patient one experienced two SAEs, consistent with an immune response. Given this, we amended the upliFTD protocol to give pulse steroids in the form of 1,000 milligrams of IV methylprednisolone for three days, followed by a transition to oral prednisone for two months. Of note, 1,000 milligrams of IV methylprednisolone is about 20 times higher dose than 60 milligrams of oral prednisone. Patients two and three received this higher level of immunosuppression and did not experience any SAEs or show evidence of a clinically significant immune response. Moving forward, future patients will receive this higher level of steroids. Let's review patient 1 safety on slide 19. Patient 1 experienced 2 SAEs, both of which were asymptomatic and consistent with an immune response. The first SAE was hepatotoxicity. Between days 14 and 21, ALT increased to 4.7-fold the upper limit of normal, with a smaller increase in AST. Other liver function tests were within normal range, and this elevation resolved without treatment. Between days 51 and 55, the ALT increased again, this time to 16-fold above the upper limit of normal, with smaller increases also observed in AST, GGT, and alkaline phosphatase, as indicated in the footnote. Notably, there was no increase in total or direct bilirubin. The patient was dosed with IV methylprednisolone, with rapid decrease in all abnormal LFTs. The second SAE was venous sinus thrombosis, also asymptomatic, which was found by MRI on day 55 post-dose. The subject withdrew from the study at week 10, so no additional follow-up data is available. Based on these findings, we amended the study protocol to, 1, increase steroids to include IV methylprednisolone on days 1 to 3, followed by oral prednisone through day 60. And 2, add additional safety monitoring that included MRIs at day 7 and day 30 and additional LFT monitoring. The Data Monitoring Committee supported continued dosing of cohort 1 with these protocol modifications, and we've added a 4th patient to cohort 1 per protocol. Turning next to slide 20, which compares the safety findings in patients 2 and 3, who received the enhanced immunosuppression to patient 1. As shown in the right table, PBFT02 was generally well tolerated and has a favorable safety profile in both patients 2 and 3 at up to 6 months follow-up. There were no serious adverse events in either patient, and all treatment emergent adverse events were mild to moderate in severity. There was no hepatotoxicity, with no significant change in liver function tests from baseline, and no evidence of any safety-related abnormalities on MRIs, and no clinically significant immune response requiring further adjustment to the immunosuppression regimen. Furthermore, consistent with patient one, there were no findings of DRG toxicity or complications related to ICM administration of PBFT02. Now let's focus on the biomarker results for Progranulin in CSF and plasma, beginning on slide 21. This slide shows the levels of Progranulin in CSF for each of the first 3 treated patients. As you can see in the chart on the left, all three patients showed substantial increases in CSF progranulin levels at 30 days after ICM administration of PBFT02, with a 3.6-6.6-fold increase over baseline. CSF progranulin levels increased to supraphysiologic levels, ranging from 10.7-17.3 nanograms per mL, exceeding the normal range from a healthy adult control sample of about 3-8 nanograms per mL, represented by the gray shaded region. Further, elevated progranulin levels were sustained at 6 months for patient two, reaching a level of 27.3 nanograms per mL, or nearly 10-fold above baseline, demonstrating initial evidence of durability of the progranulin response. We're very encouraged by these initial results from the first dose level in the upliFTD study, which exceeded our expectations based on studies in non-human primates. Turning to slide 22, we will review plasma progranulin levels. This slide details progranulin levels in plasma for each of the 3 patients over time. The gray shaded region shows the lower limit of normal range from a healthy adult control sample. As you can see, progranulin levels remain below normal levels post-dose and are fairly consistent with baseline levels, despite each patient showing substantial increases in CSF. These data are consistent with our non-human primate findings, where we saw increases in progranulin expression centrally without driving supraphysiologic levels in the periphery. Now we will summarize the interim findings on slide 23. To date, dose 1 of PBFT02 has been generally well-tolerated in patients 2 and 3, who received the enhanced higher steroid regimen. For patients 2 and 3, there have been no serious adverse events. All adverse events have been mild to moderate in intensity, and there has been no evidence of a clinically significant immune response, hepatotoxicity, or venous sinus thrombosis. Further, there's been no evidence of DRG toxicity, as measured by nerve conduction studies, and no complications related to ICM administration in any of the first three treated patients. Next, these interim data show strong evidence of target engagement in the first three treated patients, with a 3.6-6.6-fold increase in CSF progranulin levels relative to baseline at day 30. These CSF progranulin levels were also sustained at up to 6 months post-dosing. The six-month level is important, as in our clinical experience of administering AAV gene therapies via ICM, the level of protein expression achieved at month six has remained durable for all available follow-up, some of which exceeds 15 months. Achieving supraphysiologic levels at this initial dose far outperformed expectations from preclinical non-human primate studies. We're excited by the emerging data from cohort one and look forward to continuing to advance the program. We expect to initiate dosing of cohort two patients the first half of 2024. For future data updates, we expect to share six-month data from cohort one patients in the second half of 2024 and expect to share twelve-month follow-up data from cohort one patients and initial data from cohort two patients in the first half of 2025. With that, let me now pass the call over to Will to discuss future areas of study for PBFT02 and provide closing remarks. Thanks, Mark. Moving on to slide 24. Given the encouraging initial results we've seen for PBFT02 in FTD with the granulin mutation, we believe this program has the potential to impact the disease course in several additional neurodegenerative diseases. On slide 25, we will discuss the potential benefits of progranulin in additional neurodegenerative conditions. TDP-43 pathology occurs when the nuclear protein TDP-43 mislocalizes into the cytoplasm of cells, causing inclusion bodies, which are thought to lead to neurodegeneration. TDP-43 pathology is the hallmark not only of FTD-GRN, but is also found in all FTD patients with the C9orf72 mutation, 95% of sporadic ALS cases, and half of sporadic FTD. Preclinical evidence suggests that increasing progranulin to supraphysiologic levels ameliorates TDP-43 pathology. The bar chart in the center of the slide shows relative amounts of insoluble TDP-43, which is the form of TDP-43 that accumulates in the inclusions. The chart shows that a transgenic TDP-43 mouse model, shown in the gray bar, has more than twice as much TDP-43 as a normal mouse, shown in the black bar. When the TDP-43 is crossed with a mouse that overexpresses progranulin, the resulting crossed mouse, white bar, has two to three times the normal levels of progranulin, and in this crossed mouse, insoluble TDP-43 levels approach normal. In the chart on the right, the crossed TDP-43 mice who overexpress progranulin have improved survival compared to the TDP-43 mice. Based on this evidence, we believe that supraphysiologic progranulin levels could benefit patients with TDP-43 pathology, including patients with FTD C9orf72 and ALS. Moving on to slide 26, we believe high levels of progranulin have the potential to modulate Alzheimer's disease. Carriers of a particular single nucleotide polymorphism, or SNP, in the granulin gene have lower levels of progranulin and increased risk for AD. Furthermore, AD patients with the GRN SNP not only have lower levels of progranulin, but higher levels of CSF tau, which correlates with AD pathology in the brain. This particular SNP, rs5848, is quite prevalent and occurs in 30% of AD patients. Finally, preclinical evidence demonstrates that low levels of progranulin exacerbates AD, and high levels of progranulin can reduce AD pathology. Moving now to expansion opportunities on slide 27. Given this preclinical evidence and the strong initial results we've seen to date from PBFT02 in the clinic, we will be pursuing PBFT02 for the treatment of FTD C9orf72, ALS, and Alzheimer's disease with the GRN SNP. Specifically, we are starting preclinical programs that would support expansion into these three indications. In addition, for FTD C9orf72 and ALS, we will seek guidance from regulators in 2024, with the goal of achieving the fastest possible path to the clinic. Next, on slide 28, we have several anticipated milestones to look forward to. As Mark described earlier, over the coming quarters, we are well positioned to deliver multiple clinical data readouts from our FTD-GRN program. In the first half of 2024, we expect to initiate dosing of cohort 2 patients. In the second half of 2024, we will report 6-month safety and biomarker data from all cohort 1 patients. In the first half of 2025, we will report 12-month follow-up data from cohort 1 patients, as well as initial safety and biomarker data from cohort 2 patients. We also look forward to engaging with regulatory authorities in 2024 to gain feedback on the clinical pathway for treating FTD C9orf72 and ALS patients with PBFT02. In closing, on slide 29, we are excited to execute our focused strategy in support of our vision to improve the lives of patients with neurodegenerative diseases and redefine the course of their conditions. The emerging data from our upliFTD trial provided preliminary evidence that PBFT02 may be differentiated from other investigational approaches and is a promising potential therapy for FTD-GRN patients. Based on these data, we look forward to further exploring the potential of PBFT02 to address the high unmet clinical needs in multiple adult neurodegenerative patient populations. Our continued progress is supported by our established internal manufacturing and process analytics capabilities, as well as our strong cash position. Finally, I'd like to extend my sincerest gratitude to the patients, families, caregivers, and investigators in the FTD community for their continued support. With that, I'll turn the call back over to the operator. Certainly. As a reminder, to ask a question, please press star one one on your telephone and wait for your name to be announced. To withdraw your question, please press star one one again. Please stand by while we compile the Q&A roster. One moment for our first question. Our first question will be coming from Yaron Werber of TD Cowen. Your line is open. Hi, this is Joyce on for Yaron. Congrats on the data, and thanks for taking our questions. First, it looks like the CSF progranulin levels exceeded what you'd expect based on your NHP data. But on your plasma levels, it's expected that they'd be lower, but it looks like they actually were below normal controls. Can you just talk about if this is what you had expected? And then secondly, in patient two, who had six months of follow-up, are you also beginning to see changes in your other biomarkers, like neurofilament light chain, or glial fibrillary acidic protein, or is it still too early to see that? Thank you. Sure. So, let me take those in sequence. Thanks for the questions. So the first thing is, for plasma progranulin levels, these, these patients have low levels at baseline, and what we'd expect is exactly what we saw, which is no change in it, because the main effect of our vector is in the CSF. So what we saw is as expected. And in terms of the other PD biomarkers, we don't have any of those available yet. We are running them in batches, and as, as you mentioned, we have one patient with six months of follow-up. ... All All right, got it. Thank you. Mm-hmm. One moment for our next question. Our next question will be coming from Laura Chico of Wedbush. Your line is open. Hey, good morning. Thanks very much for taking the question. I have two here. On the first, how high do you actually need to go on dosing if you're already establishing a supraphysiologic response? Is cohort two really necessary, or I guess I'm trying to understand what you would learn from cohort two. Is this more a question on durability of expression? And then just a clarification, would the idea now be to include the modified immunosuppression regimen going forward, or is there any potential with a higher dose that you would need to even increase it further? Thank you very much. Sure. So let me answer the second question first. The higher immunosuppression is what we are moving forward with currently in the study. Let me go back to your first question, because that is an important one. How high is enough? Let me just outline a few things. First, here's what we definitively know. We do know that in preclinical models, supraphysiologic progranulin has demonstrated to make a difference in preclinical models of TDP-43 pathology and also in FTD-GRN knockout mice. So that we know. Now, the question is: how much is enough? What's important for us to find out is, is there a potential dose-response effect? Would we potentially see plateauing in PD biomarkers? That's what we're really looking to find. Now, in terms of cohort 2, it's very early, right? We have data on a limited number of patients. We have options for cohort two. Cohort two, we could go up in dose, we could keep it the same dose, we could go down in dose. The important thing is we are going to see the data as it comes in, and we will adjust appropriately so that we can look for a dose response. I will say one last thing, it is really exciting for us to be at this stage of the program and be able to talk about high levels. Not every gene therapy program has the opportunity to really test what these very high levels of target engagement mean. In fact, we've seen in our GM1 study that we've had to continually escalate up the dose to what we think is a very effective dose, our third dose. It's pretty exciting that we, with this program, are able to test the effects of supraphysiologic levels of progranulin, and we can achieve this already at our lowest dose. I'll toss one last question in, Will. Is there any way you can contextualize what you're observing in terms of CSF progranulin concentration versus different modalities of treatment? I'm not sure if it's possible for you to do that at this point. Thanks very much, guys. Sure. So there is certainly publicly available literature that, in patients with FTD, with a granulin mutation, that, achieving even modest increases to physiologic levels can have an effect. It can have an effect on PD biomarkers, and it can have an effect on clinical outcomes. So we, in fact, know that in these patients who are deficient in progranulin, even a modest increase in progranulin has a downstream effect. So we're very excited to see whether this supraphysiologic, supraphysiologic levels can actually push to an incremental PD and clinical effect. Thanks, guys. One moment for our next question. Our next question comes from Debjit Debnath of Guggenheim. Your line is open. Hey, good morning. This is Robert off of Debjit. Congrats on the data, and thanks for taking our question. Can you refresh us? Sure. -on the time course of FTD GRN as a disease? Along the same lines, could signals of clinical efficacy begin to be established at the 12-month update? Thank you. Sure. I mean, in terms of the time course, what we do know is that FTD-GRN, due to GRN mutations, has probably the most aggressive time course of all FTD, and it's a much more rapidly progressive course of disease. And in fact, the modeling data from the work that Adam Staffaroni has presented has really shown this very, very nicely and elegantly. That was published a couple of years ago. You know, the important thing I think in our treatment is as we understand the potential and the biomarker responses is to get into our patients as early as possible going forward. So, because we know that once the disease starts, it's a very aggressive course, and the earlier we treat, we feel will be better, which is consistent with other neurodegenerative diseases. I would say in terms of follow-up, you know, we would look to for at least a year of follow-up to really see are we making a difference in the slope of decline of these patients. As Mark mentioned, it's a pretty aggressive decline in these patients, and so we do believe that after a year of follow-up that would be appropriate to start seeing a difference. Great. Thank you. Sure. ... Again, as a brief reminder, if you would like to ask a question, please press star one one on your telephone. And one moment for our next question, which will come from Whitney Ijem of Canaccord Genuity. Your line is open. Hey, guys. Good morning, and congrats on the data. So from a TPP perspective, are you targeting supraphysiologic levels, or was that a nice surprise, I guess? Or, or how are you thinking about that, just given the kind of sub-normalization in HPs? Yeah, no, we are absolutely targeting supraphysiologic levels of CSF progranulin. Based on the preclinical data, we feel like you need to get the supraphysiologic levels to get the full potential clinical benefits of a progranulin replacement product. Got it. Okay. And then on the flip side of that, I guess, how do you think about safety, or is there a risk of supraphysiologic levels or some some cut-off or threshold, I guess, of too much being a bad thing here? Sure, sure. Great question. So first, let me say there are no known toxicities from supraphysiologic levels of CSF progranulin. From our non-human primate studies, from other studies in the literature that have tested supraphysiologic levels of progranulin in healthy volunteers, there has been no short-term toxicity. Now, there is some evidence in the oncology literature of a theoretical risk, and let me describe that. So in the oncology literature, in the microenvironment of some solid tumors, progranulin can drive cell proliferation. And so here's how we address that theoretical risk. First, the tumor microenvironment is a very different environment from the CSF of a patient with FTD. And very importantly, what we showed in the data we just went through is that our peripheral, our serum levels of progranulin are not elevated. They are, in fact, below normal. So those stay normal. In all of our patients who get this product, they have all had an MRI at baseline. Any theoretical risk out there of promoting cell proliferation in a pre-existing tumor, they're really not relevant to this program because we don't drive peripheral levels higher, unlike other programs, we don't drive peripheral levels higher, and all our patients are screened at baseline, and so they, they are not going to have a pre-existing tumor in the CNS. Got it. That's helpful. And then just last question: Do you plan to continue dosing patients in cohort one, or are you moving directly to cohort two as you talk about timing of initiation of that and just what might be gates to doing that? Sure, sure. So, as mentioned in the discussion, we added an additional patient, a fourth patient, to cohort one. In addition, after discussion with our IDMC, we are dosing a fifth patient in cohort one. There will be no delay between the patients, so up to now, for the first three patients, we've had to have a mandatory 60-day delay between patients. For patients four and five, there's no delay. It's great. We get to quickly see, generate more data, and make a decision about the next cohort. Great. Thanks very much. Sure. I'm showing no further questions at this time. This concludes today's conference call. Thank you for participating. You may now disconnect.