Good day, and thank you for standing by. Welcome to the Sangamo first quarter 2021 teleconference call. At this time, all participants are in a listen-only mode. After the speakers' presentation, there will be a question and answer session. To ask a question during the session, you will need to press star one on your telephone. Please be advised that today's conference is being recorded. If you require any further assistance, please press star zero. I would now like to hand the conference over to your speaker today, Aron Feingold, Head of Corporate Communications. Please go ahead. Good afternoon, and thank you for joining us today. With me this afternoon on this call are several members of the Sangamo executive leadership team, including Sandy Macrae, Chief Executive Officer, Mark McClung, Chief Business Officer, Jason Fontenot, Chief Scientific Officer, Rob Schott, Head of Development, and Bettina Cockroft, Chief Medical Officer. Slides from our corporate presentation can be found at our website, sangamo.com, under the investors and media section on the events and presentations page. This call includes forward-looking statements regarding Sangamo's current expectations. These statements include, but are not limited to, statements relating to advancing our program, plans and timelines for enrolling and conducting clinical trials, presenting clinical data, and opening new manufacturing facilities, our 2021 financial guidance, our expectations regarding our financial performance and sufficiency of our cash resources, and other statements that are not historical facts. Actual results may differ materially from what we discuss today. These statements are subject to certain risks and uncertainties that are discussed in our filings with the SEC, specifically our annual report on Form 10-K for the fiscal year ended December 31, 2020. The forward-looking statements stated today are made as of this date, and we undertake no duty to update such information except as required by law. On this call, we discuss our non-GAAP operating expenses. Reconciliation of this measure to our GAAP operating expenses can be found in today's press release, which is available on our website. Now, I'd like to turn the call over to our CEO, Sandy Macrae. Thank you, Aron, and good afternoon to everyone on the call. This quarter, we have continued our focus on advancing our lead programs through clinical execution, regulatory interactions, and collaboration with our partners and investigators. This morning, Pfizer's CEO announced on their earnings call that progress continues with our partner hemophilia A gene therapy product candidate, highlighting that the lead-in study for Pfizer's registrational phase III AFFINE clinical trial is now fully enrolled, which could lead to a pivotal readout as early as 2022. With Sanofi, we announced that the EMA has granted orphan designation to BIVV003, now known as SAR445136, our cell therapy product candidate for the treatment of sickle cell disease. The orphan designation was based on preliminary clinical observations submitted to the agency. We and Sanofi also received Fast Track designation from the FDA for this program. We're pleased with this progress and expect to present initial data at a medical meeting by the end of 2021. In March, we initiated our STEADFAST Phase I/II clinical study evaluating TX200, our wholly-owned CAR-Treg cell therapy product candidate for kidney transplant rejection, which we believe will be the first in-human clinical study of a CAR-Treg therapy. We were pleased to open clinical sites sooner than expected and hope to have our first patient enrolled by the end of the year. We see this study as the first step in our R&D journey towards allogeneic CAR-Treg therapies for autoimmune diseases, which we hope to develop as wholly owned product candidates in our pipeline. Our research engine has been highly productive this quarter. We continue to focus on our innovative areas, including CAR-Tregs for autoimmune diseases and transcriptional regulation with zinc finger proteins for neurological diseases. The versatility of our zinc finger technology to address challenging diseases of the central nervous system was highlighted this quarter with data publications and presentations from our tau and alpha-synuclein programs. Before I turn the call over to the team, I'd like to take a moment to acknowledge that this quarter marked one year of working in the challenging conditions of the pandemic. I continue to be so impressed by the Sangamo team's resilience and determination as our lab employees have adapted to distancing procedures and as our remote colleagues tune into Zoom calls from kitchens and bedrooms. I'm proud of the strong team we have in place to execute on the catalyst-rich year we have ahead of us. With that, I will turn the call over to Rob Schott, our Head of Development, who will provide additional details on our clinical accomplishments. Rob. Good afternoon. Our development organization remains focused on execution in the clinic, and we are pleased with this quarter's progress. As Sandy mentioned, enrollment in Pfizer's lead study in the phase III AFFINE trial evaluating our hemophilia A product candidate is complete. The purpose of the study is to collect a minimum of six months of prospective efficacy data of current Factor VIII prophylaxis replacement therapy in patients with hemophilia A to establish baseline characteristics prior to dosing with giroctocogene fitelparvovec in the AFFINE trial. Pfizer expects a pivotal data readout as early as 2022, as well as a two-year update from the Phase I/II ALTA study in the fourth quarter of this year. Regarding our Fabry program, we continue to advance the Phase I/II STAAR study, and we have recently enrolled the fourth patient. We plan to present initial data from this study in the fourth quarter of this year. In March, the EMA granted Orphan designation to BIVV003, now known as SAR445136, our sickle cell disease product candidate partnered with Sanofi. This decision was based in part on early data from three treated patients that had 52 weeks, 13 weeks, and 29 days of follow-up respectively. In a recently published minutes, the EMA's Committee for Orphan Medicinal Products determined that preliminary clinical observations, as well as the potential of long-term effects that may obviate the need for frequent treatment, suggest a clinically relevant advantage versus hydroxyurea. Last month, Sanofi announced that this program received Fast Track designation from the FDA. We find the progress on this program encouraging. We and Sanofi expect to present the initial data from the PRECISION 1 study at a medical meeting by the end of this year, which will reflect a more mature and more comprehensive data set than the early data shared with the EMA. Regarding our oncology collaboration, as part of their recent portfolio review, Kite made a decision not to submit the KITE-037 IND at this time. We are working closely with Kite to determine the path forward for KITE-037. Our collaboration remains focused on developing best-in-class oncology engineered cell therapies. Together, we believe that Kite's oncology expertise and development experience, paired with Sangamo's zinc finger platform and cell engineering capabilities, positions the collaboration well within the space. Lastly, we are very pleased to have initiated our phase I/II STEADFAST study earlier than expected. This study is evaluating TX200, our autologous HLA-A2 CAR-Treg cell therapy product candidate in patients receiving an HLA-A2 mismatched kidney from a living donor. Patient recruitment is now open at clinical sites in Belgium and the Netherlands. The primary objective is to assess the safety and tolerability of TX200. Secondary objectives include the incidence of biopsy-confirmed acute graft rejection, incidence of chronic graft rejection, and localization of TX200 CAR-Treg cells in the transplanted kidney. We also plan to evaluate the ability to reduce systemic immunosuppressive therapy, which can be associated with side effects such as an increased risk of infections or other serious conditions. We plan to enroll up to 15 patients in a group receiving TX200 and up to six patients in a control group. We plan to evaluate three doses with three patients in each dose cohort, with the option for an expansion cohort with up to six additional patients. The study will be monitored by an independent safety monitoring committee, which will give its go-ahead before moving to the next dose cohort. Patients in the TX200 group will undergo a leukapheresis to collect white blood cells prior to their transplant surgery. We will isolate a subset of T-reg cells and modify them to add a chimeric antigen receptor, or CAR, to allow specific recognition of the HLA-A2 protein present on the cells of the donated kidney. After transplant surgery and a several months recovery period, the patient will receive their one-time individualized TX200 infusion. We expect to enroll the first patient in this study by the end of this year and expect that dosing will occur several months thereafter. We believe that by directing the T-reg cells to the transplanted organ by way of the chimeric antigen receptor, TX200 has the potential to mitigate graft rejection and reduce the need for systemic immunosuppression. We see this study as offering an opportunity to demonstrate important proof of concept CAR-Treg biology in humans, as well as to better understand CAR-Treg process development. I will now turn the call over to our Chief Scientific Officer, Jason Fontenot, for additional details on these research programs. Jason? Thank you, Rob, and good afternoon, everyone. Today, I'm delighted to give you an overview of a few of our exciting research programs. We can engineer our zinc finger proteins, or ZFPs, to precisely target essentially any DNA sequence in the genome. We have invented methods to tune ZFP interactions with DNA to optimize specificity and precision, and we have developed methods to pair this targeting capability with a range of functional domains. These functional domains include transcriptional activators and repressors that can modulate gene expression without altering the genetic code, nucleases that can edit DNA sequences, and we are advancing ZFP-targeted base editors and recombinases. We can deploy these tools in vivo or ex vivo to create powerful therapies with the potential to treat significant diseases. As Sandy touched on, we are using our zinc finger protein transcription factors to develop promising therapies for diseases of the central nervous system and had some exciting preclinical data highlights this quarter. First, data from our tau program in collaboration with Biogen, published in Science Advances, showed that tau-targeted zinc finger transcriptional repressors delivered via single AAV administration selectively reduced tau messenger RNA and protein by 50%-80% out to 11 months. This without detectable off-target effects. Second, data from our alpha-synuclein program, also in collaboration with Biogen, presented at the Alzheimer's and Parkinson's Disease Conference, showed that alpha-synuclein-targeted zinc finger transcriptional repressors could significantly repress human alpha-synuclein and were well-tolerated in vivo. Finally, data from our alpha-synuclein program as well as our C9orf72 program, which was exclusively licensed to Pfizer, have been selected for presentation at the American Society of Gene & Cell Therapy annual meeting next week. We look forward to keeping you updated on these and other preclinical programs as we advance. As Rob mentioned, our STEADFAST CAR-Treg clinical study opens for enrollment this quarter. I want to provide some additional color on our research strategy with regards to our CAR-Treg portfolio. Regulatory T cells, called Tregs, have potent natural immunosuppressive properties and have the potential to be therapeutically harnessed to treat diseases characterized by unwanted or excessive immune activity. Unmodified polyclonal Tregs, a mix of Tregs which overall do not target a particular antigen, have been studied in autoimmune diseases and have been shown to be safe. We are developing antigen-targeted CAR-Tregs and believe that our approach may overcome the limitations of polyclonal Tregs by directing the Tregs to the relevant diseased tissue, where they will be activated and expanded upon CAR binding with the target antigen. The antigens targeted by our CAR-Tregs can be linked to the disease etiology or simply be localized in the diseased tissue. For example, in our multiple sclerosis program, we are programming CAR-Tregs to target myelin oligodendrocyte glycoprotein, or MOG. MOG is expressed specifically in the central nervous system, and similarly to a GPS, we will aim to drive our MOG-specific CAR-Tregs to expand at the site of inflammation, where they could suppress the pathogenic immune reaction responsible for MS. In our inflammatory bowel disease, or IBD program, we are targeting the receptor for the interleukin IL-23, or IL-23R, which is known to be expressed at sites of ongoing inflammation in the gut and is involved in IBD pathology. In both programs, we're investigating multiple target antigens. We're using our zinc finger genome engineering platform to develop allogeneic Tregs, edited Tregs from healthy donors ex vivo to produce off-the-shelf CAR-Treg cell therapy. We are also investigating the potential use of induced pluripotent stem cells, or iPSCs, as a renewable source of large quantities of Treg cells. We are making progress on these programs, working first at developing efficient and proprietary CAR structures, and then on obtaining proof-of-concept preclinical data both in vitro and in vivo. We look forward to presenting our preclinical data in due course. I will now turn the call over to Mark for an overview of the financial results. Mark? Thank you, Jason Fontenot. Good afternoon, everyone. As Aron Feingold had mentioned previously, our financial results for this quarter are available in the press release issued this afternoon, which can be found on our website. This quarter, we invested in the advancement of our clinical programs, moving forward our preclinical research pipeline and continuing to build our in-house manufacturing capabilities. We ended the quarter with approximately $630 million in cash equivalents, and marketable securities. We believe that our balance sheet remains strong and will allow us to reach several important R&D milestones, including the potential submission of the BLA for our Hemophilia A product candidate. Turning to 2021 full-year guidance, we would like to reiterate the guidance we provided in our prior call. We continue to expect non-GAAP operating expenses, which exclude estimated non-cash stock-based compensation expense of approximately $30 million, be in the range of approximately $255 million-$275 million for the year. I'll now turn it back to Sandy for closing remarks. Thank you, Mark. I'd like to conclude by saying that we're pleased with the progress this quarter across our development and research organizations, and continue to believe we have the balance sheet strength to execute on our R&D milestones. Our manufacturing team continues to advance our in-house cell therapy manufacturing facilities, which we expect to be operational by the end of the year. We look forward to key milestones and catalysts by year-end, including initial data readouts on sickle cell and Fabry, as well as a two-year update in hemophilia A. Operator, please open the line for questions. Thank you. Our first question comes from the line of Luca Issi from RBC. Your line is now open. Oh, perfect. Thanks for taking the question. This is Lisa on for Luca from RBC. Just wanted to ask, we saw yesterday that Avrobio will no longer be able to pursue an accelerated approval pathway for Fabry disease, but they may need to run a phase III trial head-to-head versus standard of care Fabry enzyme. We're just wondering what your reaction was to that news, and how does that influence your development strategy going forward for your gene therapy products? Thank you. Thank you for your question. Each company has their individual discussion with the agency. Bettina, you've been working on Fabry for some time now. What was your take on that announcement? Yeah, sure. Sandy, thank you. Well, first of all, what we are doing is we're currently focusing on pressing full quarter ahead on enrolling the Fabry study. That phase I/II STAAR study, and as you've heard Rob mention, we have dosed three patients and have enrolled a fourth patient who we hope to dose soon. We are looking forward to sharing initial data readout in Q4. Our study design includes collecting biomarker data, and as we've mentioned in the past as well, we will conduct kidney biopsies at the appropriate time. The study is currently unaffected by the recent regulatory updates that you're referencing. For sure, we are engaging with the agency. At this point, as you'll appreciate, it's too early to share an update on that front. Thank you, Bettina. Great. Thanks for taking the question. Thank you. Our next question comes from the line of Maury Raycroft from Jefferies. Your line is now open. Hi, this is Kenneth Chan on for Maury Raycroft. For TX200, we noticed the trial initiated a bit earlier compared to the 4-2 press release. What work needs to be done before the patient enrollment second half of 2021? Thanks. Thank you for your question. Yes, we were pleased with the clinical operations group managing to initiate sites. I think they've done a remarkable job in the time of COVID. Now it's simply a matter of moving forward and enrolling patients and preparing for the dosing of the patient. This is the first time that we have dosed a patient with CAR-Treg. We're going to take care, be prudent, make sure we have the right patient and the right manufacturing process to be able to drive forward and do this well. Hopefully show that CAR-Treg's potential matches everyone's excitement around this area to allow us to move into many autoimmune conditions. Thanks. Thank you. Our next question comes from the line of Geoff Meacham from Bank of America. Hey, guys. It's Aspen on for Geoff. Thanks for taking the questions. Just two quick ones from us. First off, Sandy, I would love to hear your thoughts on the current regulatory environment, specifically with respect to CBER. Any sort of reduced communication, or are you feeling any sort of shift in mentality from the agency with any respect? Then secondly, just looking for a little bit more clarity on the Kite's decision not to submit the IND. Just wanted to see if you had any additional feedback you can share with us. Thanks. Let me take the more philosophical one, and then I'll pass it on to Mark for the business discussion around Kite. I saw this week that Peter Marks was given an award for his service to advancing medicines, and it feels totally appropriate. We have had a great relationship with CBER. They are doing a difficult job and are flexible and thoughtful. I often get asked, has the regulatory environment got harder or are they asking more? I would reflect it the other way around. The cell and gene therapy is this wonderful concept that we all are so excited by. Now what we're meeting is the reality of what it takes to have a medicine approved. It's about ensuring your manufacturing is good, your cell process is good, your science is good, the clinical trial is good. It's not surprising that some of the excitement is now meeting reality. We take these stages extremely seriously at Sangamo. We invest greatly in CMC regulatory interactions and manufacturing and are comfortable and confident that the agency hasn't changed its opinion. I'll pass on to Mark now for Kite, Gilead. Mark, do you want to talk about that? Sure. As Rob reiterated, Kite made the decision not to submit the 037 IND at this time. The team is going to look a little bit closer to understand a potential path forward. This has been made in the context of the emerging early data from two competitors that were ahead of the 037 program. Also in the context of the data that Kite has on hand with the startup product, which the focus is really to drive something which would be a best-in-class alternative and would allow for an expansion of the utilization of these products. The goal is to continue to apply Kite's expertise in the development of oncology paired with our zinc finger platform and cell engineering capabilities to really look for opportunities to develop and advance best-in-class oncology engineered cell therapies. Thanks, guys. Thank you. Our next question comes from a line of Yanan Zhu from Wells Fargo Securities. Your line is now open. Hi. Thanks for taking my questions. I have a question regarding TX200. I see that it's enrolling in Belgium and Netherlands. Wondering, is there any difference in terms of the immunosuppression that is used for the renal transplant procedure, any difference between Europe and the U.S.? If there is some difference, would you also plan to open an IND in the U.S. to have a more relevant treatment procedure for the U.S. application? Thanks. Thank you for your question. That's an interesting question because renal transplant and how you treat it differs a little from country to country. Bettina, would you feel comfortable to talk about that? Yes, for sure. I mean, Sandy, you've said that there are differences from country to country in addressing immunosuppression in renal transplant. Our study, as we've mentioned, has recently initiated, and we are enrolling in these first two countries. You've mentioned the Netherlands and Belgium. This is something that we will hopefully be able to update you in the future with. I might also add, this is Rob Schott, that there's often institution-to-institution differences in immunosuppressive therapies, and you can even find differences within institutions between investigators. We rely on the investigator judgment with respect to immunosuppression and therapy consequent or following the TX200 therapy. Got it. That's very helpful. Maybe a follow-up on the C9orf72 program. Could you talk about the potential advantages for using the zinc finger protein transcription factor versus using a gene therapy that delivers shRNA, for example, to knock down a target gene? Thank you. Sure, would be happy to. Jason, can you help us with that one? Sure, Sandy. I think the key difference is really about the platform technology, about our platform technology and our ability to fine-tune the interaction of our zinc finger proteins with the designated target. We have very fine control over that, and we have the ability to identify a zinc finger protein that can accomplish what we set out to accomplish with the therapy and not have any off targets. I think that there's a major difference between our ability to do that with zinc finger proteins and competitors. Beyond that, from a clinical point of view, the RNA therapies seem to need to be given frequently. We would hope that episomal expression of a transcription factor would give a long-lasting effect. It seems to do it in animals. Until we get into humans, we won't know for sure. The promise this gives to patients of a once and done therapy is really important. These are dreadful diseases, and if we can address them with our transcription factor, we will fulfill our mission and promise. Great. Thanks for the color. Thank you. Our next question comes from the line of Gena Wang from Barclays. Your line is now open. Hi, this is Swapnil on for Gena Wang. Thanks for taking our question. I had a Fabry question. Since looks like Gb3 reduction in kidney biopsies could serve as a surrogate endpoint, is it safe to assume, like you're predominantly focused on recruiting patients with kidney defects? Do you think that FDA would require longer-term follow-up to monitor eGFR to grant full approval based on the FABRAZYME update? Thanks. Thank you for your question. The agency is doing its very best, in my mind, to make the pathway forward for Fabry clear and tractable. What they have said is Gb3 reduction in the kidney with the commitment to have a long-term eGFR benefit is a pathway to approval. Therefore, I think that understanding the effect on the kidney is important. We are recruiting patients that are on enzyme replacement therapy, are naive, and are pseudo-naive in the current study. We are looking to show a biochemical effect, and then we will move towards doing kidney biopsies. I think the patient population is wide-ranging from patients that've already had renal damage to those that are undamaged. What my reading of the literature tells me is that this is an important consequence to the patients, and that patients show renal damage from very early on. In amongst that population that we're already recruiting, there will be patients with renal consequences. Let's wait. Let's see the results at the end of the year, let's work out a sensible path forward. Okay. Thanks for taking our questions. Thank you. Our next question comes from the line of Ritu Baral from Cowen. Your line is now open. Good afternoon, guys. Thanks for taking the questions. It's actually me. I wanted to ask you about the rationale for picking HLA-A2. On slide 11 of your corporate deck, you note that 21%-26% of renally transplanted organs are HLA-A2 mismatched. First of all, I wanted to make sure that 21-26 was renal, was kidneys, and not just organs in general. Second, in your comments today, between MS and IBD, it seemed like you were implying that you had sort of multiple targets per program pick auxiliary targets. I was wondering if you also were thinking that had an auxiliary target for renal transplant and what proportion of the organs that might represent as well. I'm going to ask Jason to speak to this because in Jason, we recruited someone that did some of the fundamental work on Tregs. For the kidney transplant, it is about 20% have mismatches, and that means that there is a substantial population of patients who are getting an HLA-A2 mismatch that our CAR-Treg can be taken to by its GPS to find the HLA-A2 and activate it no matter what the other mismatches are in the renal transplant. That's the beauty of this system. Jason, do you want to talk about our general strategy for Tregs? Sure. Thanks, Sandy. Yeah, I think one of the things that's critical to keep in mind here is that Sangamo is really pioneering this effort. The work that we're talking about is the first opportunity to test engineered CAR-Tregs in humans. The opportunity to use the A2 mismatch presented just a very elegant way to approach the tissue targeting because we know that the A2 molecule will only be present on the transplanted kidney by virtue of the design of the trial. That's the real reason for using the A2 approach. I think one of the really exciting things about the CAR-Treg platform, especially in regards to the subject of your question, which is the antigens that we pick for CAR targeting, is that we are able to pick targets that, as I highlighted, are connected to the disease etiology or simply just tissue-specific targets. That's a real advantage for us versus some of the problems that we see in the CAR-T field and in oncology, where identifying targets that are unique to the cancer has become a real challenge. We're able to either use something that is connected to the disease pathology or simply find something that is an antigen that's expressed in the tissue where we want the Tregs to localize to. As we're gaining a huge amount of knowledge and understanding by advancing the TX200 program, and we intend to build upon that knowledge in refining which targets we pick for future programs. That's why we're keeping the opportunity to pivot to different targets by advancing multiple targets in each of these indications. Just a quick follow-up on that and the STEADFAST study and following up on a previous question. As we think about the two secondary endpoints that you have on slide 12, especially the ability to reduce immunosuppressive therapy. Given that the regimens, I guess, can vary from center to center, how will we quantify reductions in immunosuppressive therapy as part of this protocol? The reason I'm asking is it's my assumption that this might be the first needle to move. Is that a correct assumption? Or could acute graft rejection generate the first of the efficacy signals between those two bullets? The advantage of modern medicine is patients rarely lose their kidney. The way they avoid that is with immunosuppression, which comes with all- Right kinds of health consequences. This is a cutting-edge, state-of-the-art study that has to allow normal standard of care by the investigators. Of course, we would love everyone to do the same thing, but the study would not progress without that. We will gather the information from this. We'll gather information from renal biopsies. We'll understand about the Tregs. We'll watch what they do, what happens when they reduce their immunosuppression, and we'll use that to design the next study and the next part of this program. Got it. Thanks for taking the questions. Thank you. Our next question comes from the line of Benjamin Burnett from Stifel. Your line is now open. Hi, this is Kelly Breese on for Benjamin Burnett. Thanks for taking our questions. Had one quick one about TX200. I was just wondering if you could provide any additional color about the starting doses that we may expect to see at the first look at data. If you could provide any other color on it. We haven't talked about the doses. We're going to do three doses. It will be some number of cells that we will talk about later. We haven't said anything up to now. Okay. Awesome. Thanks for taking our question. Thank you. Our next question comes from the line of Andreas Argyrides from Wedbush Securities. Your line is now open. Good afternoon, and thank you for taking our question. This is Andreas Argyrides on for Liana Moussatos. With regard to the ASGCT abstracts, have the respective partners selected a lead candidate yet from the library generated? When might we see these assets enter the clinic? Thanks. For our partner programs, that's down to our partners to talk about them. We work closely with them. We sit on steering committees with them. The rules of the relationship is it's for them to talk about it. Okay. How should we or investors look at the abstracts being presented from a scientific standpoint? Thanks. From a scientific standpoint, I think is very fair. I want to assure you that our partners are excited by the progress of the CNS assets, and we look forward to speaking more about them in the future. Okay. Thank you. Appreciate it. Thank you. Our next question comes from the line of Debjit Chattopadhyay from Guggenheim Securities. Your line is now open. Hi, guys. Thanks for taking my question. This is Aron on for Debjit. We noticed from the Fabry clinical trials entry that the patients must have cornea verticillata, acroparesthesia, anhidrosis, or angiokeratoma to be included. Can you tell us any estimate of the percentage of Fabry patients with those symptoms, and why those particular symptoms? Bettina, this feels like one for you. Yes. Thank you, Sandy. As you rightly point out, ClinicalTrials.gov, we have listed the inclusion and exclusion criteria for our Fabry STAAR study. The symptoms you listed, cornea verticillata, acroparesthesia, anhidrosis, angiokeratoma, these are symptoms that are classic of Fabry patients. Patients need to have at least one of those symptoms, if not more, to be able to be enrolled into the study. That is to ensure that beyond the documented diagnosis of Fabry disease, we are enrolling patients who do have the underlying condition. Okay, great. Thank you. Thank you. At this time, I'm showing no further questions. I would like to turn the call back over to Sandy Macrae, CEO, for closing remarks. Thanks so much. This is Aron. I'll take that. Thanks once again, everyone, for joining us today and for your questions. We look forward to keeping you updated on our future developments. Have a great afternoon. This concludes today's conference call. Thanks for participating. You may now disconnect.