Hello, everyone. I'm Max Skor, a Biotech Analyst with Morgan Stanley. Before we get started, for important disclosures, please see the Morgan Stanley Research Disclosure website at www.morganstanley.com/researchdisclosures. With that, I'm happy to introduce Steve Harr, CEO of Sana Biotechnology. Thank you very much for joining me today. Max, thanks for having us. Really appreciate it. So maybe just to get started, we'll give you the stage, introduce Sana's story, maybe set up recent progress, and what we should focus on going into the end of the year. Sure. I'm sure everybody here recognizes we'll make forward-looking statements, and like you, I have my own little risk factor. Please read our 10-Q for looking at those risk factors. We started the company around the idea that one of the most important transformations that will occur in medicine over the coming 20 years or so is the ability to engineer cells. We wanted to do this in a way that allowed us to go after diseases that are highly prevalent, with scalable platforms that could access patients broadly. We chose to go after two problems. Excited to say, shortly we should be getting going on studies for them and really understanding their impact on human health. The first one is, if you transplant someone else's cells into your body, your body will see them as foreign and try to reject them or will reject them. It has been the major limitation for transplant medicine for decades. How we went after the idea of trying to hide allogeneic cells, a transplant from immune recognition. It turns out that the technique we use seems to hide them, at least in some cases, not only from allogeneic, but also autoimmune rejection. Probably the most visible or potentially most important program that we are working on is a one-time functional cure for type 1 diabetes. Type 1 diabetes is actually a pretty simple disease from far away, which is the immune system gets confused and attacks and kills the pancreatic beta cell. The beta cell is the only cell in our body that makes insulin. Before the advent of endogenous insulin about 103 years ago, patients just starved to death. Their cells couldn't get any sugars over the course of several months. Since then, people have done a lot better, but they still are still not great. Even with the best therapy today, your average type 1 diabetic will live about a decade shorter than someone without it. To put that into perspective, that is about the same for a 20-year-old being diagnosed with type one diabetes as being diagnosed with breast cancer or HIV. During that time, it is a very complex life, right? At every meal, every time you exercise, every time you get a little bit sick, you are trying to adjust your insulin. These people deserve something better. If you take a step back and say, okay, the missing cell is the pancreatic beta cell. I am going to go back and forth between beta cell and islet. Just think of it as an islet is the beta cell plus its support structure. About 25 years ago, a guy named James Shapiro, and others have followed, started isolating pancreatic islets from recently deceased people's pancreases. It turns out it works very effectively. They are transfused in the liver, and people have lived for decades without any insulin. So normal blood glucose is no insulin. The challenge is it is not a very replicable supply source, right? There is a lot of variability. It is not very scalable. People have to be on extraordinary immunosuppression, like an organ transplant. There just are not that many people for whom the risks of immunosuppression are less than the risk of diabetes, right? But there are thousands of people around the world who have gotten this. Over the last several years, others have begun to show that you can take pluripotent stem cells, either embryonic stem cells or induced pluripotent stem cells, iPSCs, and you can grow them and mature them into pancreatic islets. There seems to be a more replicable outcome. It is kind of working on almost everybody. Two, it seems to be that it is probably more scalable, and I do not think we have answered that question for sure. But people are still on lifelong immunosuppression, and again, so they limit the impact. Over the last several years, what we have shown is we can make some gene modifications. First, we showed in vitro, then in mice, and then in non-human primates, and we showed it in people. We actually did this in type one diabetic, published in the Journal of Medicine, that we can gene modify these islets, transplant them into a person with type one diabetes, and they will survive and function. The last update in the New England Journal of Medicine is at 14 months. So no immunosuppression, cells doing really well. So now you have all the component parts together for a one-time curative therapy for type one diabetes. What we have is a gene-modified iPS cell-derived islet. So we've made a handful of gene edits. We made a master cell bank, we've grown them, and then now we'll differentiate them into islets. We've been working hard at this. I think we're almost there. Our goal is to get the IND cleared this year and start our phase I study this year. I'll go through this, but you should know pretty quickly if this works or not. I'm sure you'll ask me questions, but I think it's probably worth a second question before people get bored of me rambling. We have another platform, though, and that is, our goal at that point was to go after another big problem, which is you can do more or less anything you want to a genome in a Petri dish. The hard part has been delivering it into the cells in the body. So we wanted to develop a platform that would allow us to go after the challenge of being able to deliver to any cell in a specific, repeatable, and with any payload way. We seem to have made some real progress on that. So our most advanced program is in vivo CAR T cell. We've been at this for a while. We have a platform that we believe gives us some very specific advantages we can get into versus others. They've got a little bit ahead of us, so I hope it does play out, that it's been worth the time to make a best-in-class therapy. I'm quite confident if you were a non-human primate, this would be the best-in-class therapy, and whether or not that's true with a human, we'll have to see. But again, our goal is to get that study started soon and start generating data and get that out in the not-too-distant future. Okay, great. Let's start with the type one diabetes program. Stepping back, you talked about the New England Journal of Medicine paper. The follow-up UP421 data showed continued islet cell survival and insulin production without immunosuppression through 14 months. What do you expect the October presentation to add to investors' understanding of durability, immune evasion, or cell function? Zero. I said this from the beginning. There's nothing that will get you after about a month from the immune system. So these cells are going to live until they die. When they die, it will be because of something related to these cadaveric islets, most likely. When they live, it doesn't mean that our cells, which are stem cell-derived islets, will live in the long run. If they die, it doesn't mean our cells will die. We got immune evasion, and now we need to put these stem cell-derived islets in and ensure that they last for hopefully decades for people. Unless something really surprising came up, like there's some new twist in the immune system that killed these things, I don't think you learn anything as you watch this for longer. I've kind of been pretty clear on that for a while. Okay. I don't view any update around us learning that things are still alive as being material. I would view if they died and that it was because of immune response, we would tell you. Otherwise, just assume they're doing fine. Okay. Let's fast forward then to progress towards starting the SC451 phase I/II trial. We can break it out. I can ask specific questions, but what are the gating factors? What are the challenges? If you could lay that out for us, that'd be great. Historically, the biggest challenge for us, it took us years to figure this out, was trying to make a genomically stable GMP master cell bank. I'll explain what that all means. It turns out, we gene edit a pluripotent stem cell. We knock two genes out, we knock two in. As we did that, what we'd find as we grew these in, because you start with one cell, and you could grow every patient, let's just say it's around a billion cells as a dose. Every thousand patients is a trillion. To go after a disease of 10 million people, you need quadrillion cells. As we grew up the number of cells, we would start to see mutations arise, and essentially it's DNA repair enzymes because you put things in growth media that selects for cells that grow quickly. The cells that grow quickly are those that don't stop to fix their genome. The biggest challenge is doing that when we did it. Once we did that, it's actually been pretty rapid, and we have three work streams we're working our way through. Number one is just being clinically ready. You have the clinical trial protocol aligned with everybody outside the company, regulators, physicians, others. Then in this case, because we're delivering this product, we send some live cells into a hospital where they have to be stored, processed, and then actually put into the muscle of the patient. We need to make sure that was replicable and good. That was part one. We feel very good about where we are there, and in particular, we had a collaboration we signed earlier this year with the Mayo Clinic. They've been quite helpful ensuring we did that in a replicable and hopefully reproducible way across sites. Number two is there's all kinds of non-clinical studies that get done, the things that are normally done, GLP tox studies, biodistribution efficacy, some things that are specific to what we do, genomic stability, because you don't want cancer-causing mutations in these cells. Then another one is we have a safety switch we put in so that in case something did go wrong, we could kill the cells. That's preliminarily all done. We don't have the final study reports in our hands yet, but I think that can be off all of our worry lists. The third thing is manufacturing. These are complex medicines, and we need to both lock a process and then transfer it in from our research labs into a GMP or good manufacturing practice manufacturing suite, and then have it done by their hands, not our scientists' hands, but their employees' hands. We're finishing that. Hopefully that goes very well. We'd like to believe we're going to file this IND, get it cleared, and start our Phase I study this year. We don't know if we'll dose anybody this year. I think that's another question, like we want to make sure it's the right patient at the end of the year around the holidays. But we'll hopefully get all that done soon. Okay. Can you talk about the trial design, the number of patients you anticipate enrolling, and just timelines in general? Yeah. I think that there are three things you are trying to learn. Well, let's just say you always try and learn safety. That's the most important aspect of any phase I study. So let's put that in. There are two main safety things to be worried about, at least as far as we know from afar. One is when you put in these stem cell-derived islets, some of them don't live. They don't engraft. This will always happen when you put cells in, and they're full of insulin granules when they release. We need to make sure we don't have severe hypoglycemia or low blood sugar in the short term. Super easy to deal with if you have it, hopefully, which is just IV sugar. The second thing is, in the long run, tumors, and that's going to take many patients. So safety. Then what we want to know is, first off, does the technology or what we've seen, the immune evasion in the end of one study we did, transfer into these gene-modified stem cells? If that occurs, I would argue the majority of the risk is out of the program. Because we're going to transplant cells into a patient with a pre-existing immune response against beta cell, or islet cells. With no immunosuppression, they should be rejected in a matter of days. If they're not, if these cells are living, let's just use as a marker a month out, they're probably going to live for years and years and years. So that's question one. Does that happen? I think that that will be super important, and if it does happen, it will be a very important event for our company. The second is we're not just trying to make a great technology, we're actually trying to make a drug. The goal of the drug is normal blood sugars or euglycemia with no more insulin shots and no immunosuppression. If we use the experience of others, that may take us a quarter or two to ensure we have potent enough cells and we get the efficacy we want. So, that could happen again pretty early in the year. The third thing is this a consistent result? Is this going to happen in more or less everyone? Is it going to be some subset of patients? That may take us a bit longer to figure out, but we like to think we can figure that out maybe as we move through next year. So, our phase I study set up is around a dozen patients. We can kind of flex it either direction. We want to make sure we have a good solid dose and that these things really work, and I think then it's pretty straightforward to move into a registration study, assuming it all works as we hope it does. How have interactions gone with regulators? Everything on track in that regard? Yes. Okay. It's an important field, I think, from a regulatory perspective. They understand the unmet need. It's a very vocal patient group because they haven't had anything really novel in a century. I think with the human data that we have in this N of one experience, there's a lot of curiosity about how well that will translate to people. We've found that regulators around the world in many jurisdictions have been helpful in helping us navigate questions and the path forward. Maybe you can comment a bit more on the- That does not mean they're easy. It means they're transparent. The deal you signed with the Mayo Clinic earlier in the year, the implications of that and maybe looking out further, any strategic partnership you think would be valuable, or are you interested in that? I'll start with the Mayo Clinic's been just a tremendous partner to date in the collaboration with them. I have to say, from my perspective, it's exceeded at least my expectations. In the very near term, they were trying to help us with two challenges. In the long run, we hope they can help us with more. One is really de-risking this period, this black box, from the time the drug product leaves our hands until when the patient leaves the hospital. There are elements of product storage, there are elements of product preparedness. We're sending it in a media, to keep it alive for a while, they have to concentrate the cells down, because you don't put all that media into your muscle. There are elements of just delivery, getting the cells into the right muscle at the right time, and with the right needles and all that stuff. Then elements of taking care of the patient. So we wanted to make sure we're standardized in a way that it could be reproducible across many sites. It's been really great for that. They also then came with a bit of cash for us. There was a $25 million investment in the company at a premium, which is helpful because we're an early-stage company where our cost of capital is high, and that was quite helpful. Those are the two things that came with it to date, and I think we're both optimistic there'll be more as we go forward. Then view on potential strategic partners going forward. We'll have to see. I always think of this, if you knew the answer to these four questions, you would know how this movie plays out with this drug. One is, does it work? You'll learn that very quickly. Two is, can we figure out how to scale manufacturing? This is a disease of 10 million people. There are 500,000 new patients a year. If we somehow cure 100,000 people per year, the prevalence pool will still be growing. So we have to figure out scale. Then the third is, can we figure out a commercial model for a curative therapy of a highly prevalent disease? Those are the three big giant macro questions. The fourth one is, how do we finance our company through all that? So we know big pharma partners can help with the latter. I don't think they can help us answer the question, does it work? Because the drug's kind of being made. The cards are on the table. We just haven't been able to flip them over yet. So we'll have to see if they can help us with these others, or if it's just, again, never say never because you never know what the financial conditions are of companies. Certainly, if they can grow the pie for us, that's very, very attractive. If they can de-risk these kind of existential questions for us, that'd be very, very attractive. It's not clear yet that anybody can, because the questions haven't been answered, not that we're better than they are, it's just the questions haven't been answered. It would be great to have a bigger pie with lower risk and more capital. Those are all good things, but we'll see if anybody can ever do that. I kind of like the idea of taking this forward a while on our own, but that isn't always the right answer for patients. We'll do what we think is the right thing for the therapy and for all of our stakeholders. Okay. Not pressing you to look too far ahead, but the cadence of updates. Should we expect by the end of the year, we'll get a press release that the phase I trial has started, then first quarter. I think investors have been very clear to us that IND clearance is material on their mind, just given the complexity of this medicine and how hard it's been for us to make it. Above and beyond that, we'll figure it out when it happens. But I think that's something that's very material to us, so we'll make sure that that's something if it happens, I guess, make sure. We'll be waiting for that press release. Yeah. All right. But I don't think we want to give a blow-by-blow of everything that happens because it puts unnecessary pressure around things that sometimes the better answer is a week later. Right. That's fair. We want to make sure that we get the best answer. Okay. Maybe we can pivot to the rest of your platform, SG293. If you can introduce it, where you're at, and I can ask some specific follow-up questions. Sure. This is an in vivo CAR T program, leveraging a platform we call the Fusogen platform. This particular drug makes a CD19-targeted CAR T-cell which we intend to initially develop in the setting of blood cancers, in particular non-Hodgkin lymphoma out of the gate, with a goal if the safety profile allows it to move into things like autoimmune disease, where I think it could be, if the safety profile allows it, really transformative. We did three things that are different than the field in making this platform, and we'll see how they play out as being clinically important. The first assumption that we made was that you want exquisite specificity in delivery, meaning you only want to go to T-cells. I think many others have taken a different view, and I would tell you one of our board members had a different view around this, and so it's not like it's crazy, which is you just want to get enough of the genetic material into your target cell, the T-cell, so you can make enough CAR T-cells and that's your major thing. Our view has been, though, that for safety reasons, for reasons around immunogenicity, and even just for manufacturability, just because T-cells are a small number of the cells in your body, that you want to be exquisitely specific. I think we confidently can say we've established that within the context of the technologies that are out there. I can get into why, if you want. The second is that you want to have a signal that integrates into the target cell. What that means is we put in the cell DNA, and that DNA goes into the chromosome of the target T-cell. When you CAR T-cells you might make 100 million of them, if you're really good at it in a patient. But you and I have probably 100 billion B-cells, and if you have B-cells plus tumors, you have hundreds of billions of cells that have to be killed. Therefore, your CAR T-cell is going to have to go through multi-logarithmic expansion or growth to kill all of the cells. If you don't integrate it into the chromosome, the signal won't go to the progeny cell. mRNA, there's a lot of really smart people who spend a lot of money, and they could be right. I'm not saying we're right. These are just the assumptions we made. Specificity matters. You want to do integration over mRNA. Smart people are making a different bet, and integration has its own safety issue. It's got at least a theoretical idea that could go in the wrong spot of your genome. The third thing that we made a bet on is that you want to dissociate entry of your genetic material from activation of the T-cell. What you've seen is that all the other people who are doing these virus-like particles, more or less, are trying to use CD3 as the way that they get to T-cells. That has led to a new toxicity, which is a peri-infusion toxicity, which in some cases has put people in the ICU on blood pressure and has actually led to people getting, around the time of effusion, very high-dose steroids, 20 mg of dexamethasone, which if you've ever taken steroids, it's a lot of steroids. With these three things, we think because we've dissociated those two things, we can get entry without overactivation. We can get the DNA going into the progeny cells, and we only go into T-cells, and that will give us a clinical advantage. We need to see that that's true in humans. The next step is to get into humans. We've been working towards starting an investigator-initiated trial in China imminently. We had some things that slowed down a bit. There was some adverse publicity around, in other studies, some people who died in China, and I think that that's just led to people dotting their I's and crossing their T's. I don't think in any way it's going to impact our ability to get this done. Last week we told people instead of data later this year, it's probably going to be in the first half of 2027. It's still coming at us. If that works in the lymphoma setting, we will expand to other cancers. If the safety profile allows it, we will go into the autoimmune space where I think, again, the benefits can be profound. There's no lymphodepleting chemotherapy. There's all kinds of things that are maybe different than other. If that also works, we have a second drug targeting BCMA that's ready to go into human testing, but we're a capital-constrained small company, and we figure we don't need to do two drugs in the same platform until we see the first one work. Okay. That's fair. Could you just comment on what would constitute meaningful early proof of concept across the CAR T generation? Is it safety, durability? Kind of set the stage for what we can expect in the first half of next year. I think you want to see a reasonable safety profile with complete responses, like elimination of the tumor. I think we have something better. For those of you who don't know, I was in the CAR T space for a while, an old company that did this. One of the things that we weren't always sure of, particularly in the lymphoma setting, was whether a complete response would translate into a durable complete response or maybe like a functional cure. It turned out that if people's CAT scans or PET scans, PET CT scans were negative at 6 months, they almost never recurred. That's a long time to wait as you're going through dose escalation studies to figure out if you're at the right dose. We have a new technology. It's ctDNA, or it's kind of circulating tumor DNA. This really allows you early to understand, is a patient likely at a dose and with a therapy that's likely to lead to a durable complete response? I think we learn pretty quickly. Do you have complete responses with undetectable ctDNA in a drug that is reasonably safe? If you have that, it's going to be a really important drug. The bar is probably you want to do as well as autologous CAR T cells, right? If you're that higher bar of that, the ease of use of this, the lack of lymphodepleting chemotherapy, which comes with a lot of toxicity, is probably pretty attractive, right? If it's better, that's a no-brainer. Or if it's moderately worse, maybe you compete with T-cell engagers, or you have to figure out if you really have a drug, right? I mean, that's kind of at least a higher bar of what to think about. Okay. Before moving on to maybe some macro questions, I wanted to pivot briefly back to diabetes and just ask if SC451 data are positive, what would regulators need to see before Sana could transition into a registrational program, particularly around patient population, safety database, efficacy, durability, et cetera? Yeah. I do not know the answer to that question is the clear answer. We have not engaged any regulator on the planet around what a registration study will look like. I think that from my own perspective, what we would want to see is a few things. One, I think we have kind of outlined there would be three different periods of manufacturing. There is good enough for phase I. We have that, but just barely, right? There is good enough for we call an early commercial launch. To do that gets into number of patients, and you want to have reasonable gross margins, right? You have to have that in place at the start of your registration cohort because you are not going to be able to change your manufacturing process meaningfully while you are doing that. We have some work to do to get that. We have made a lot of progress over the last six months. I am way more optimistic than I was at the beginning of the year that this is going to be readily doable, but we are not done, to be clear. The third will then be like tens and tens of thousands of people, hopefully at very attractive gross margins. To get to the process lock on that phase and that registration study is likely the rate limiter of the registration cohort, right? You are going to have, as I said, do you have any short-term safety issues to deal with? As far as we know, which again, you never know till you know, the major thing we need to ensure is that we can deal with the short-term risk of severe hypoglycemia. Assuming we can do that, which seems readily doable, then at least as I think about it, the other risk would be long-term, do these things ever cause tumors, right? You need lots of people for long-term follow-up. I think the registration study should be relatively limited, I do not know if that is true or not, with pretty meaningful post-marketing follow-up, but we will have to see. Then it is a manufacturing question. I do not think there is a lot in there that we need to grapple with. What we want to make sure of is that we have a consistency of result, and if it is inconsistent result, that we understand what patients it is more or less likely to work in. We want to get the dose reasonably right. It is hard to imagine you can overdose this stuff. I mean, it is glucose-sensitive insulin secretion, but because we will be capacity limited for years and years, if we give people 2X the dose, we will help half as many patients as we might otherwise do it, so that is not helpful. Need to make sure we get in that dose kind of right. We want to make sure of the manufacturing process. In terms of patient population, the patient population we are looking at is very broad. It is not everybody, but it is most people over 18 with type 1 diabetes. We may change most to even more as part of our phase I. I would like to think we would get into a pediatric population if this works in a relatively urgent fashion. Start with 16 plus, 12 plus, and then you get a little more. It is clearly parents and those kids really want something like this. It's a big burden for them. We're going to go through all that, but I don't think any of them are gating necessarily the starting of a registration study. Okay. Just in regards to financials, could you just talk about your cash runway, capital allocation, any color around that? Yeah. At the end of the second quarter, we had $160 million. We've said that gets us into the middle of next year, assuming we continue to run the business as we do today, which is our goal. I don't think you can cut your way into making these things work, right? The goal, I'd just say, we'd like to bring more money in the company in the not-too-distant future. We're not urgent about it or anything like that. I'd like to think with reasonable clinical data, it's a good time for us to be thinking hard about financing the company and/or partnerships, everybody that understands kind of where we're allocating that cash, what we need, and what the inflection points are. We have the capital we need to get through the next set of value inflection points, which is, do these drugs work? Again, if they do, we're going to need to make sure we do more. If they don't, it's going to be messy, right? Neither one do. But we'll figure that out if it happens. Our hope is that they both do. In terms of capital allocation today, the vast majority of it goes to this type 1 diabetes project. It is an enormously complex drug, right? This is an aggregation of novel transplant immunology, CRISPR gene editing stem cell biology and really difficult scale manufacturing, in one drug. It has to be done. We can't outsource these things. These things are done inside of the company. But we've done it now, hopefully, and at least we can turn the card over, and if it works, we'll get the privilege of playing out the next hand. Great. With about four minutes to go, if you can entertain a couple of macro questions. How is the rise of China innovation changing your competitive positioning, your thoughts on R&D, or maybe how BD plays out long term? Well, we've developed these medicines ourselves, and they're enormously complicated. We're just going to stick to our knitting and do what we do, and we're not looking to bring in other molecules or anything else in near term. I presume that China's been wonderful at innovating on the sciences of scale and manufacturing, that as we go through, if this thing happens to work, that we'll have to make sure that we continue to focus on scale and cost of goods, so we can deliver this at a reasonable value to patients and payers around the world. I think they've been very thoughtful in innovating around how to get proof of concept in humans at a reasonable level of regulatory burden and cost. Some of those things, I think, are being applied in the United States. We're in the process of trying to figure it out. More of them need to be. W e will never be able to apply them all. We have the challenge in that many of these companies have subsidies and things from them, and we have the other benefit, which is why we're here. There's this really robust and rich and deep capital markets expertise that resides in the United States, and that's part of what we hopefully have the opportunity to leverage in making important medicines. Great. Question number two, AI implementation. Is Sana taking on AI, leveraging it internally? What are your thoughts on the future? We're not taking it on. I mean, it's pretty powerful stuff. Sorry, bad choice of word. Yeah. Leveraging it. We do. I divide it into three major categories as we think about it. One is just knowledge extraction, where I think it's super powerful for that. I think most people use it. There's no excuse for showing up to a meeting and saying, "I don't know what we're talking about today. Haven't heard or learned about this." You can always show up with a reasonable level of knowledge. They can also help people accelerate their understanding of complex things with what's known in the field pretty rapidly. The second would be operating efficiencies, and that's in areas that relate to how we run our business. Whether that's in finance. A lot of the G&A functions or some elements of clinical trial work. I think we're getting some of that. It's helpful. I don't think it's mind-boggling helpful, but it's helpful on the margin. The third are things like creativity enhancements, like really making novel therapies and things because of it. That's not an area we currently have really gotten much out of it. Partly related to, we have what we think we need, and we just need to understand it in humans. We're exquisitely focused on that. But that's how we've divided it and where we're getting what we can out of it. Okay. In the last minute, anything Please don't send me any AI-generated emails, like that kind of stuff. Okay. That's fair. Those are just delete it, right? Anything I missed? They're not true productivity enhancers because no one reads them, right? Yeah. Last minute, anything I missed or anything you'd like to call out? Well, I'd like to just highlight, we've been at this for a while. We went out and when I started the company, the goal was to do something that if it happened to work. There were two goals when we decided what to do, broadly. One was if it happened to work, we wanted it to be transformative, not something incremental. The second is for it to be complex and complicated. That had to do with just the type of people that are attracted to it. It's also just what's worth doing. I think we nailed finding those things, and it's been hard. We've had some setbacks along the way, and we've made a lot of progress. We're now sitting here, and I was saying to someone, sometimes it's felt a little like we're waiting for Godot. Like Godot's going to show up. W e will be in a position, we believe, to deliver to you, to patients, and all our stakeholders an understanding of what these drugs do over the next several quarters. Most importantly, we're really focused on trying to understand is the technology that we've really proved in humans already to work translate into this gene-modified stem cell-derived islet because if it does, a cure for people with type 1 diabetes becomes absolutely inevitable. That's our focus. That's what we really want to deliver for patients. We want to deliver for others, and we're hopeful we can do it. Great. Well, thank you very much for joining us today, Steve. Appreciate it. Thanks. Thank you, everybody in the audience.