Morning, everyone. I'm Jason Coloma. I'm the CEO of Maze Therapeutics. First of all, I'd like to thank the Jefferies team for inviting us to this year's conference. I'd also like to acknowledge our forward-looking statements. At Maze, our mission is simple yet ambitious: to harness the power of human genetics to transform the lives of patients. An emphasis for us is chronic kidney disease. Kidney disease is a silent killer. Over 800 million individuals globally suffer from this disease. It's the ninth leading cause of death to date. In some countries, there is a four-year waiting list for kidney transplants, and there has been little innovation and no precision medicine approaches for kidney disease. That is where Maze fits in. We develop small molecules using our genetics approach to really be able to focus on kidney disease. Now, our small molecules start with MZE829. That's for APOL1-mediated kidney disease. There are at least 1 million individuals in the U.S. alone who can benefit from such an approach. We are enrolling our phase II right now and have an intent to have clinical proof of concept data in Q1 2026, where we could be the very first company to describe clinical proof of concept in broad AMKD patients with or without diabetes. Our second program, MZE782, is focused on SLC6A19, also a small molecule approach. Now, we are developing the therapy potentially in PKU, where we showed clinical, if you will, proof of mechanism for this particular approach in September. We were also the very first group to show clinical proof of mechanism in chronic kidney disease in September, highlighted by our recent events and presentations at the large American Society of Nephrology just a couple of weeks ago. Based off the strength of our data last September, we intend to start two phase IIs, one in PKU, the rare metabolic disease, and a second program in chronic kidney disease also in 2026. 2026 will be a big year for Maze Therapeutics, where we intend to show, again, clinical proof of concept in broad AMKD in Q1 of 2026. With our second program, we intend to start two phase II programs, one in PKU and one in kidney disease in 2026. Now, I'd like to turn our attention to MZE829 in APOL1-mediated kidney disease. The genetics of APOL1 kidney disease was known for a very long time, over a decade, but unfortunately, no one really understood the function or mechanism by which APOL1 was causing disease. Our group was one of the first groups to identify the relationship and understanding of the mechanism on how APOL1 was really causing kidney disease in these patients. Moreover, we have developed what could be a best-in-class approach, could be one of the very first disease-modifying therapies for these patients. Now, APOL1 kidney disease, for investors, four things to highlight. Number one, that we know at least one million individuals have the variants in kidney disease, and at least 250,000 individuals could benefit from a therapeutic approach. We have developed a small molecule that could be once-a-day dosing, best-in-class, and that we have a dual mechanistic approach, which has not been described by other compounds in development. We recently, if you will, have highlighted our phase I data. We presented that data last year's ASN event, which is the large kidney conference, that gives us the confidence as we continue to enroll our phase II and plan to unveil data that could be the first time clinical proof of concept is demonstrated in that broad AMKD patient population in Q1 2026. The evolving, if you will, regulatory landscape of understanding how kidney disease can have a path to registration and that pivotal study, we plan to enact planning on that on the heels of that data next year. Now, we know a lot more about the patients who have APOL1 kidney disease. It disproportionately affects the Black community. We know that they're younger. So those that have the variants that cause disease, they're younger than those that do not have the variant. About what they do is they clinically present about, if you will, below the age of 50. Kidney disease is often associated with an elderly population. These patients are younger. We know that they have, if you will, more aggressive disease in the sense that they progress to end-stage renal disease as well as into dialysis about 10 years earlier, the non-APOL1 kidney disease patients. We know, unfortunately, that the current therapies are not effective in this patient population. They are younger, they progress faster, and they are not responding to standard of care, and there are no approved therapies for these patients. Us and other sponsors hope to develop what could be the very first disease-modifying therapies for these patients by treating the underlying cause itself, which is to target APOL1 gene directly. Now, at least 250,000 individuals have enough proteinuric disease where they can benefit from a therapy. What we know now is about 60% of those do not have diabetes, and about 40% have diabetes. That's important to highlight in the sense that we intend to be the first group that can show clinical proof of concept in patients that don't have diabetes as well as those that do not, really being able to, if you will, address the majority of patients who can benefit from this approach. Fortunately for us, clinical proof of concept has been demonstrated on APOL1, albeit in a smaller, more defined population called FSGS, which is great because the target itself has been de-risked in terms of the biology. What we intend to show is a broader set of patients who might benefit from that therapeutic approach in Q1 2026. Now, diving into the mechanism itself, we know what APOL1 is doing in the sense that there are two variants, G1 and G2. There's only two that can cause the disease and causes a toxic gain of function that ultimately results in APOL1 itself acting as a channel or a pore in the podocyte. Now, the podocytes are found in the glomerulus, which is the primary filtering unit of the kidney. What you can see here in the right panel is the fact that you have an overexpression of those pores, so you have many more of them. Ultimately, you have them ungated in a sense that they're actually just creating holes in those particular podocytes, resulting eventually into that nephrotoxicity or the toxicity and killing and damaging those cells. At minimum, you want to be able to block those ungated channels from acting in that way, resulting into that toxicity. What we learned about MZE829 is we also have a dual mechanism, which differentiates itself from all other compounds that are in development in the sense that we're not just blocking the pore, we are also disrupting the assembly of those pores from forming to begin with. That is important because the turnover of that particular, if you will, protein is high. It is under an hour, and it highly turns over in the podocyte, such that you not only want to block it, you want to be able to disrupt the assembly of it. What we know now is the fact that no other compound that's been described to date in the literature has the same type of effect, and that allows us to not only differentiate in terms of the molecule, but address the broader population, including those that may have diabetes. Now, our phase I results, the key takeaways are the fact that we have linear dose proportionality. You can see the two panels here that show our SAD and MAD data. We have the half-life of about 15 hours. This will be a once-a-day drug. We also had high confidence in the dose that we were selecting to bring that into our phase II that basically describes that we can at least get to an EC90. That's important because not only do you want to hit this target as hard as possible, you want to be able to disrupt the assembly of that pore. That particular data set allows us to give us the confidence exactly what we wanted to see in order to be able to start our phase II. Now, our phase II study is called HORIZON, ongoing enrollment, on track to deliver the data in Q1 2026. What we are doing in this case is we are screening for the genotype. You have to have one of the G1 or the G2 variants that cause this disease. We treat for three months, and then we follow for a month. What we're trying to do is, again, be able to try to expand the population to a broader set of patients that allows us, for the first time, potentially show that clinical proof of concept. Now, what we want to do in terms of the minimum data, in terms of the threshold that we are saying what could be clinically significant and would demonstrate clinical proof of concept in these patient populations, is a 30% reduction of uACR relative to the baseline. This would be significant in the first time being able to show that type of clinical effect. If we're able to do that and we see the data that we would like to see in Q1 2026, we can start and initiate our planning for phase II-B, if you will, which would be more of a registrational study next year as well. Now, in terms of our next program, MZE782, what we're really focused on here is being able to develop this particular opportunity for PKU patients. What we know in terms of PKU to date is that untreated, basically, patients resolve inability to have these multiple, if you will, issues, including these neurocognitive, neuropsychiatric detriments that really affect individuals across the board. What we know today is that the therapies that have been approved, even to date, are not able to address the entire spectrum of disease. We know at least 60% of the patients are not on therapy to date because they're inadequate. Our approach, which could be the first oral substrate reduction therapy approach, could work across the entire spectrum of the PKU patients. In terms of PKU itself, we know that this could have broad impact. We just had data in September that demonstrated that we could have proof of concept, if you will, a best-in-class molecule in being able to have substrate reduction in PKU. We know there's at least 58,000 individuals across the world who could benefit from this type of approach. We showed best-in-class principles relative to any other molecule that had been described in the literature to date. We plan to initiate phase II in 2026. Now, based off of what we knew from the existing literature, we knew that what you want to be able to do clinically is, at minimum, be able to reduce plasma Phe in the blood, which is the, if you will, the neutral amino acid that causes disease, as that is the regulatory endpoint for approval for PKU patients. Now, in healthy volunteers, what you want to be able to do is be able to show an increase in excretion of urinary Phe, as it translates very well in terms of the plasma Phe reduction in patients. What we're able to do is be able to show that effect in the healthy volunteers and compare that to previous studies that have been described in clinical development to show that we could be potentially best in class. If we can do that, we would be able to show that we have the ability to work across the entire spectrum of disease. Our data in phase I supported advancement into phase II. The key takeaways is that we had a larger healthy volunteer study. We, again, showed very strong, if you will, PK, PD response. We had a safety tolerability profile that really supported the ability to forward this into phase II. We showed, if you will, best-in-class principles in particular in the urinary fee biomarker relative to anything that had been described to date. To highlight that, a previous study had shown at a particular dose that they had a tenfold increase in urinary fee relative to the baseline. That is the dash line that you see here on the slide. That was where the original benchmark was in terms of where you wanted to show some level of pharmacodynamic effect. What we had shown here, of course, is that we had exceeded that tremendously in the ability to do that, demonstrating that we have best-in-class opportunity here and the ability to maximize, if you will, the ability to reduce the plasma fee such that we can show clinical benefit eventually in PKU patients. They had shown a tenfold increase in urinary fee previously. We showed, on average, a 40-fold increase in urinary fee, demonstrating the ability that we could maximize the opportunity across the entire spectrum of disease. Now, we're equally excited about this concept of SLC6A19 in chronic kidney disease. We were the first group to identify the genetic relationship of looking at this particular gene in the context of chronic kidney disease. What we had shown is that certain individuals were really protected from developing end-stage renal disease and even transitioning into dialysis if they had a particular variant of SLC6A19. We use that information to really be able to address what could be, if you will, the next anchor in terms of a way that we can develop chronic kidney disease medicines going forward. Now, in terms of what we were able to do with chronic kidney disease, we see this opportunity as potentially being the next SGLT2, which has become an important anchor in the way that kidney disease is treated today. We have demonstrated in vivo proof of concept demonstrating that we can be superior in particular models relative to SGLT2. We had been able to demonstrate genetic analyses that really support our work. Ultimately, in our proof of mechanism study and our phase I that we presented in September, we were the first group to show clinical proof of mechanism that this potentially could have a renal protective effect, which is indicative of all approved chronic kidney disease medicines to date. Based off of the totality of that data, we are progressing in 2026, starting with a clinical proof of concept study in chronic kidney disease. This data here was an important milestone for the program in the sense that it demonstrated for the very first time in vivo proof of concept in a kidney model and put that into context with SGLT2. What you can see here in terms of the graphs, one is the ability to lower proteinuria in that particular model. You can see in the particular bars in green our agent, and in the orange, you can see that compared to an SGLT2. Even at an EC50 relative to what we were doing in terms of exposure, we were able to not only reduce proteinuria better than SGLT2, we were also able to reduce, if you will, injury markers in the kidney called K IM-1 and others that demonstrate that we could have, if you will, even a more superior efficacy in these particular models. Moreover, what's interesting is that there's a potential for combining with SGLT2s. You can see that in the black bars on both of the graphs as well, where you not only see this additive effect in the proximal tubule injury markers like KIM-1, but you're also able to see that basically get to a normal state in the proteinuria when you combine SLC inhibition with SGLT2 inhibition. Really remarkable in the sense that we might be able to really have an impact in ultimately improving kidney health. What was interesting to us, based off the genetic analysis that we had been sharing with nephrologists, as well as some of the in vivo proof of concept data that we had shown to particular nephrologists, what they encouraged us before we started our phase one was to be able to collect a biomarker serum creatinine such that you can calculate eGFR, which is a measurement of kidney function. Why did they tell us to do that? They told us to do that because what they knew across all medicines that had been approved for chronic kidney disease, whether it be a RAAS, an ARB, SGLT2, even NMAs, which is a new modality, if you will, for kidney disease, all of them had shown this phenomenon of having an initial eGFR dip, which is represented here in the graph, which was indicative of long-term renal protection, especially when you compare that to placebo. It is a little bit counterintuitive to see an eGFR dip initially, but what that did is really be able to slow the rate of decline following treatment over time, which was really indicative of renal protection. They saw that nephrologists knew that they had seen that across multiple different classes of agents, including SGLT2. If we were able to see that in our phase one data, even in healthy volunteers, on top of our genetics, our in vivo proof of concept data, this would really be able to reinforce what we had seen in our particular analyses. For the first time, we are the first company to demonstrate the ability to show this eGFR dip, indicating that this may have renal protective effects in patients when we bring this into the clinical proof of concept study. What you see here in terms of the graph is we see that there is a dose-response relationship here on the right graph, really being able to see that type of drug effect. To ensure that we see that drug effect, you see that on the left graph, which is when we pull the healthy volunteers off of drug, you can see that the eGFR bounces back up, indicative of the fact that this truly is due to the therapy itself. The last thing is what you see in that orange bar is we compare that and contextualize it to SGLT2, represented by EMPA here. You can see that the range of what we are doing in terms of eGFR dip is quite in line with SGLT2. One, not only do we see a dose response, two, we know that it is due to the treatment itself based off of the fact that we pull the individuals off of the treatment and you still see the effect. Lastly, we see that in about the same magnitude as SGLT2, again, reinforcing the fact that this could have renal protective effects as we bring this particular therapy into our proof of concept study. Now, as you think about what we're planning for 2026, this will be a big year for us. We have our initial clinical proof of concept data in APOL1-mediated kidney disease. We could be the very first company to demonstrate clinical proof of concept in a broad set of patients with or without diabetes. The second thing to highlight is we've put the bar in terms of success at 30% reduction of proteinuria relative to baseline. If we're able to do that, we could be initiating planning for a registrational phase II- B3 study next year. Now, in terms of some of the things to highlight for investors, one is that we do have the product candidates really be able to transform the way that kidney disease is treated today, starting with MZE829 and the ability to show clinical proof of concept in that broad patient population, trying to show that we can show that 30% reduction in uACR. We also are initiating off of MZE782 and the strength of the data in September, the ability to start two phase IIs, one in PKU, the second in CKD. The last is the fact that we've been able to demonstrate, if you will, the ability to not only be one of the few IPOs this year, we also had a financing in September that enables us to be well capitalized to deliver on all of our particular data catalysts that I've been highlighting throughout the presentation. Our vision at Maze Therapeutics is to become one of the next generation precision medicine companies that allows us to develop small molecules in kidney and metabolic diseases. We have the product candidates, we have the team, and we are well capitalized to deliver on all of our particular milestones that have been highlighted to date. Not only do we have the ability to develop those two molecules, we are just getting started. Our scientists are hard at work back in San Francisco being able to develop additional small molecules in both kidney and metabolic diseases that allow us to provide not only additional pipeline that we may develop ourselves, just like the two programs I described today, but could be leveraged, if you will, for partnerships as we've been able to demonstrate even with our Pompe program with Shionogi, demonstrating that we can not only be able to advance our programs ourselves, but also through partnership. Now, with that said, I'd like to thank you all for attending today. I'd like to thank our team back in San Francisco and thank you to the Jefferies team for having us at this year's conference.