Good morning. Welcome. I'm Eric Joseph, Senior Biotech Analyst with JP Morgan. Our next presenting company is Akero. Presenting on behalf of the company is CEO Andrew Cheng. There'll be a Q&A session after the presentation. Just raise your hand if you have a question. We'll bring a mic over to you. For folks tuning in via the webcast, you can also submit questions via the portal. With that, Andrew thanks for joining us. Good morning. Thank you Eric for having us. So 2025 is going to be a very exciting year for Akero. And I'd like to begin by talking a little bit about the year ahead of us. So let's move on to the first slide. This is our Safe Harbor Statement, which is in very small 8-point font. And I will not read, but I'm going to pause so that I can be compliant with Safe Harbor and legal disclaimers. Let's move to the next slide. So when you think about the things that have taken place over the last year or so for Akero, is that we've really made the transition from a phase 2b company, which we had both primary endpoint results for our Phase 2b F2, F3 pre-cirrhotic study in 2022. And then in 2023, we had our primary endpoint for our Phase 2b cirrhotic study. Those have progressed in that we had the 96-week readouts last March for the pre-cirrhotic study. And upcoming next month, we'll have the 96-week readout for the Phase 2b cirrhotic study, which we call Symmetry. In that time frame, we've also started our phase lll program, which was initiated with two studies, which we are calling SYNCHRONY as part of a three-study package. The first two studies, SYNCHRONY Histology and Real World, began in the Q4 of 2023. And yesterday, we very excitingly announced that we completed enrollment in the first of our phase lll programs. That is SYNCHRONY Histology, which is a, excuse me, SYNCHRONY Real World, which is a non-invasive study looking at patients who are F1 through F4 in a randomized double-blind placebo-controlled fashion, 600 patients over 52 weeks. And these patients are followed non-invasively. So this is the primary goal of this trial, which is one of safety and efficacy. But it is one which the patients, although they did have a biopsy to come into the study because the patients came from screening from SYNCHRONY Histology, there's not a second biopsy. They all be followed in a non-invasive manner, looking at both efficacy and safety. And we, importantly, because the study was fully enrolled, we announced yesterday it will read out in the first half of 2026. And as we've done in previous studies, as the time draws closer, we will refine that time point. Because you can imagine that with the first patient yesterday and one year later will be quite, we can narrow that window. Why don't we move on just by way of background, just to understand what efruxifermin is. Efruxifermin is a bivalent FGF21 analog that is an Fc fusion protein that we, the founders, Tim Rolph and Jonathan Young, in-licensed from Amgen in 2017. That really is the basis for Akero. Importantly, FGF21, as you may recall, native FGF21 has a very, very short half-life that doesn't make it suitable to be a drug. What the FC fusion protein has done is it's extended the half-life to between three to four days. It also is modified in the FGF21 portion, mostly at the C- terminus. You can see modifications at the 171 and the 180 residue. You can see that it's important that it enhances the binding to the co-receptor beta-klotho, as the cartoon designates. The interaction of EFX in order to transmit a signal is a trimeric interaction. The C- terminus of FGF21 binds with the co-receptor beta-klotho, though, anchoring it to the cell surface. And then the N terminus is able to bind the FGF receptors, whether it's 1C, 2C, or 3C, to transmit the signal through the transmembrane domain, as diagrammed in the cartoon there. Importantly, what we've seen through our clinical trials is that we've seen sustained pharmacodynamic effect through two years in our FGF21 portion through 36 weeks with our F4 patients, which we'll follow up on soon in the 96-week readout. When I turn now and talk a little bit about the cirrhotic patients, because that's what we're reading out next month. And just as a reminder, we borrowed this slide from an FDA presentation. It's from Patel and Gastroenterology, but the FDA is used to it. So we thought we would use it as well. It just highlights the importance and, unfortunately, the acute medical need for patients who are cirrhotic. In red is a Kaplan-Meier curve, and you can see that the 50% mortality for patients who are diagnosed as F4 outside of liver transplantation is, unfortunately, 50% mortality at five years, and it is dramatically different when you look at the other pre-cirrhotic stages. If one were to go to the right on the Kaplan-Meier curve, you can see that the, let's say, F2 or F3 patients, that same 50% mortality occurs at about 15 years, so really, there's a pretty stark difference in terms of the outlook for patients who are pre-cirrhotic versus cirrhotic, and that really highlights the need to have therapeutics for this population, for which, unfortunately, there is no approved agent for this population. Turning now to the Symmetry study, which is our phase ll trial. As a reminder, it's a randomized double-blind placebo-controlled study looking at two doses of efruxifermin, 28 or 50 milligrams versus placebo, in patients who are compensated cirrhotics. That is, they're F4 Child-Pugh A patients, so the key inclusion criteria really is listed here, that they're biopsy-confirmed F4, stage 4 MASH, and compensated cirrhotics with either type 2 diabetes or two of the components of the metabolic syndrome. The primary endpoint read out at week 36, and I'll talk about that momentarily, and as a reminder, we're now in February reading out the two-year data. That is week 96. Keeping in mind that we're not powered for this endpoint. The primary endpoint was at week 36. There are key secondary endpoints. I won't read through all of them, but they're listed there that we revealed also at week 36, but we'll also be looked at at week 96. Turning to the next slide really talks about the bar chart on the left. We can see that these are the week 36 results at the primary endpoint. That is for patients who had a one-stage improvement of fibrosis without worsening of MASH. It demonstrated that the 50 milligram arm demonstrated a 24% one-stage improvement of fibrosis in contrast to 22% for the 28 milligram dose and placebo at 14%. As noted in the bars, neither of the two EFX arms reached significance when compared with placebo. As you'll see in a follow-on slide, these are among the best results ever seen in this population. We also conducted a sub-analysis on the bar chart on the right. This subgroup looks at patients who were either diagnosed for greater than six months prior to study entry as having cirrhosis or cryptogenic cirrhosis. That is, those patients with the most advanced form of Child-Pugh A, those who have sometimes just referred to as burned-out MASH. That is, that they have relatively little liver fat because much of their liver has been replaced by, and their hepatocytes have been replaced by fibrosis, and in that population, we see that roughly the efficacy is largely the same, 22% for the 50 milligram dose. But interestingly, the efficacy drops for the 28 milligram dose and, interestingly, for placebo down to 3%, so it's something as when we looked at a relatively large subgroup, more than approximately 60% of the patients in the readout, we see some differences when it comes to their response rates in the placebo and the 28 milligram arm overall, looking at that primary endpoint. I mentioned earlier, looking at, this is one of our landscape slides. And I just call your attention to this is a placebo-corrected slide. So when one looks at the other compounds that have been studied for F4 NASH, you can see a variety of different companies. Two of the studies come from my former company, but also different mechanisms, some FGF21 as well as LOXL2, GLP-1 from semaglutide from Novo. And there is one unfortunate similarity, putting all the studies to the right, is that really the results were largely very placebo-like. And in some cases, placebo had a better response than some of the patients treated with active. If you look at the semaglutide results or the Bristol-Myers Pegbelfermin results, placebo exceeded the active arm. And you can see that's represented by the negative number. So clearly, this has been a difficult field to have successful trial results. I mentioned earlier that you see the Akero efruxifermin results, although not statistically significant, as I pointed out earlier, were the best results seen in the field to date at about 8% and 10% placebo-adjusted effect sizes. One of the challenges when one looks at biopsy overall is that the liver is among the largest solid organs in the body. Yet we're looking at a biopsy using a 16-gauge needle, and you're looking at 10 or 11 portal tracts. And it's quite small. How does this look when one looks at the entire liver looking non-invasively? You can see that at this study. You can see that when one looks at some of the more reliable non-invasive measures, was the ELF score or composite score, liver stiffness or Pro-C3. You see important improvements in both the L score, statistically significant versus placebo, and in Pro-C3 as a marker of inhibition of new collagen synthesis. Patients treated with EFX at either dose have responded very well. You see this is consistent with what we've seen in prior pre-cirrhotic studies. This is an example of one of the patients. I think this is something that we did not fully expect to see. That is, that this is a patient histologically that had a three-stage improvement of fibrosis. They came into the study, and you can see the baseline biopsy on the left, which is F4. You can see the extensive bridging fibrosis as well as a nodule on that slide, and after 36 weeks of treatment and a mild weight loss of about two kilograms, this patient, this 69-year-old woman, managed to be F1 after nine months of treatment, so this was a remarkable improvement. We had two patients in each of the arms or one patient in each arm, two patients total have two-stage improvement of fibrosis as well as a three-stage improvement of fibrosis, so really, when we look at this, we see the potential for EFX to reverse fibrosis in patients who are cirrhotic, something which some physicians and investors had questioned, was that all possible? But the histologic evidence is here on this slide. At the same time, looking at non-invasive measures, so this is a NAS score on the right-hand side. If one looks at histology and fibrosis markers, we'll focus on the NAS score at the top. You can see at baseline, the patient had a NAS score of five with 122 across the categories, and after nine months, the NAS score was zero, so really, on both measures, looking at the liver biopsy for fibrosis as well as NAS score and looking below, when one looks at non-invasive markers, see improvements in Pro-C3 as well as FAST, so again, a very consistent picture for this patient, both histologically as well as non-invasively, so when one thinks about this, one of the questions I often get asked is, well, that's great that this patient has done well at 36 weeks. How will this read out at the two-year point, at 96 weeks, which will read out next week? Why do you think things will improve? And to that, we look at some of the results from previously I mentioned in the Harmony study. So as a reminder, similar trial design, different color scheme, but we have two doses in a randomized double-blind placebo-controlled trial of F2, F3 patients. All the patients were biopsy-confirmed. Again, the primary endpoint slightly early at 24 weeks, but then at two years, we had a follow-on biopsy. And importantly, what we see is that when one looks at the one-stage improvement of fibrosis, which is on this slide, these are the results sort of shadowed for both doses. You see statistically significant results for both doses at week 24 versus placebo, roughly 40% versus 20%. But interestingly, when one looks at what happens at 96 weeks, we see a real expansion, especially at the 50 milligram arm of the response rate, going from 41% to 75%. And then really, when one looks at this, it really tells us that longer dosing has improved the response. The question is, what is the color around that longer dosing? Are these the same patients, different patients? When one looks, oops, let's see if I did that wrong. So here we go. Going to the next slide is that we've broken this down within the bar charts of the 75%. I think it's the easiest to look at there. You can see that we have a group of patients who had a sustained response, 11 out of the 21 patients of the 75%. Those patients had a response at week 24, but also maintained their response out to week 96. Interestingly, roughly half the patients, 10 out of the 21, were new patients, people who were not successful at week 24, but then with increased dosing became successful at week 96. We're encouraged that the antifibrotic effects and the benefits of this compound aren't. They don't plateau at the six-month period. They can be maintained and extended. That's one of the strongest points for us that we think that longer dosing does matter for this compound, and it can be manifested in histology. When we break this down and look at the subgroups, I think to put some numbers around it, the top box really looks at patients who had the sustained response. You can see for the 50 milligram dose, that number is 92%. 11 out of the 12 patients who were successful at week 24 maintained and continued to be successful. We have a durable response for those patients. And then for the people who were non-responders at week 24, you could see 63% of those, of the 10 out of the 16, became responders. We continue to bring in new successes. Longer dosing does benefit patients regardless whether they were successes at week 24 or not. Now, one of the other questions is, when one looks at the slide, you can see that we've expanded the breadth of the patients who are responders. But what happens to patients who are already responders? And can the depth of response increase? And this is a measure of two-stage improvement of fibrosis. In this slide, you basically see that very point, is that using the same schema, you see roughly 15% of the EFX-treated arms had a two-stage improvement of fibrosis at week 36, excuse me, at week 24. But by week 96, you can see that's increased to 36% in the 50 milligram arm and 31% in the 28 milligram dose. So again, now longer dosing has done both things. It's both expanded the breadth of response, but also increased the depth of response. So one thinks of a 36% two-stage improvement of fibrosis. That is a number, quite honestly, is quite strong. And that's, as you've seen on the slide, highly statistically significant when compared with placebo. Let's turn now to the patients who have F3 fibrosis. One of the reasons we bring this up is investors often ask, are a lot of these responses driven by the easier-to-treat patients who have F2? There's less fibrosis. Maybe all of the patients who have a two-stage improvement are driven by the F2 patients. We've just narrowed the analysis to focus on the F3 patients, the hardest-to-treat pre-cirrhotic patients. You can see the response rates at week 24, 29% and 28% on the treated arm versus placebo, and when one expands out to week 96, you can see that roughly 68% of the F3 patients have responded. Yes, smaller than the average of 75%, but again, very robust response. One thinks of more than two-thirds of patients by two years who are F3 at baseline having a response of one-stage improvement of fibrosis, and you can see that's in contrast to 14% on placebo. So again, that response is highly statistically significant. And when one looks at this, you can see that breaking this down into this similar slide of the patients who are F3 who had one stage or more of fibrosis, you can see on the 50 milligram dose, actually, the majority of those patients, eight out of the 13, had a two-stage improvement of fibrosis, even though they're F3. So the harder-to-treat population, yet they still were able to have a two-stage improvement of fibrosis with extended treatment. So when one thinks about the totality of the data, it's this response rate, which is 75% one-stage improvement of fibrosis, is not driven exclusively by the F2 patients. It's shared almost equally between F2 and F3 when one looks at the pre-cirrhotic patients. One of the questions that's come up mostly from physicians or investigators is that we all recognize how important biopsy is as it's the FDA and EMA regulatory standard for approval, but at the same time, clinically, biopsies are not used as often, so what the pushback and the question for us is, when you think about this compound being approved, how will non-invasive measures be able to guide us? Because that's what patients aren't eager to have biopsies probably comes as no surprise, but how can we follow these patients, and what non-invasive measures are helpful, so these are a data set, and I'll walk you through. It's a little bit complicated that we presented at last fall's AASLD meeting, the American Association for the Study of Liver Diseases, in San Diego. What we've done is taken the patients who have had one-stage improvement of fibrosis, and that's one of the circles. And then we've wanted to see how much overlap is there with common non-invasive measures. The non-invasive measures we've used are liver stiffness, which is generated from a FibroScan. And it's a liver stiffness response of greater than or equal to 30%, which is often correlated with clinical benefit, and an L score of reduction of greater than or equal to 0.5. And what you can see is that on the far left in placebo, of the patients in our study, roughly half the patients, 47% of the placebo patients, had none of those attributes, not a single one. And then when you think about those that had overlap, as you can see with the overlapping Venn diagram, you can see that the placebo response, none of them had more than one. So even for the patients who had had a one-stage improvement of fibrosis, they had neither liver stiffness improvement nor LSM. And what that really shows is that the placebo response is likely a representative of sampling error, the liver being heterogeneous, and that there are times when one part of the liver may be F2 or F3 or F1. And when you see it improving, it's not really correlated with the non-invasive measure, which is a representative of the whole liver. Now, in contrast, what you see, let's just move to the far right in the 50 milligram dose, is that when one looks at the patients who had none of those measures, meaning that in contrast to the placebo, 47%, that didn't occur. Every single 50-milligram patient had at least one of those measures, whether it's fibrosis improvement on histology or either the ELF score improvement greater than 5% or the FibroScan improvement. So it's not so common that things are black and white in clinical studies, but this is one of the most important. And then when one looks at the patients that had all three events, roughly 40% of the patients had that event. So improvement of fibrosis correlated and overlapped with both non-invasive measures. And you can see the 28-milligram is in between. So we have a nice dose-response. But what this data helps highlight is that for EFX, the histology does correlate well with whole body, whole liver, excuse me, non-invasive measures. And it's an important guide when one looks forward to when this compound's approved, how will physicians use this? You could see that they could use either or both of these non-invasive measures to follow their patients. Let me turn now to the next slide. Turning to safety, this is again important. Importantly, Importantly, nobody died in the study to date. There were serious adverse events that were seen anywhere from 9%-16%, depending on the groups. The number of patients that had a drug-related serious adverse event was one in each of the EFX arms, so just a small number of patients. The reasons are listed on the slide. The most common adverse events were GI in nature, diarrhea, nausea. But keep in mind, relatively few patients discontinued for either of those two events, despite the number being roughly about 35%-40% for each of those adverse events. So overall, the drug has been relatively well tolerated. You can see that the discontinuation rate is less than 10% after two years when one thinks about these events. And that's an important thing when one interprets this slide to look at the duration of study because it's cumulative. So other safety measures to look at: blood pressure. There's no statistical difference in either systolic or diastolic blood pressure at two years when compared to placebo. There are markers of hematologic function and hemostasis, whether it's platelets, bilirubin, or the composite scores of MELD and CP, Child-Pugh. They remain stable. Progression of cirrhosis was balanced across the group. It was relatively small, fewer than five patients in each arm, and roughly similar between the groups. There were no significant changes in bone mineral density at one year with the EFX arms compared to placebo. We did see at two years significant reductions of between 3% and 4% at the lumbar spine and reductions at the 50 milligram dose only, not at the 28, less than 3% at the femoral neck. It's important to keep in mind that some of the differences were aided by an increase of about 8.8% to 1% in the placebo arm. In terms of fractures, the fractures were relatively similar between the groups. The worrying fracture of vertebral fracture was only seen in the placebo arm at the first lumbar vertebra. Lastly, I'll just conclude. As we think about the SYNCHRONY phase lll programs, which we're in the midst of, on the far right is the SYNCHRONY Real-World Non-Invasive Study. As I mentioned earlier in the presentation, we've completed the double-blind enrollment. We're very excited about that with the first readout in the first half of next year. For the SYNCHRONY Histology, the registrational biopsy study, that is, the enrollment's ongoing still, but we expect the readout to be in the first half of 2027. We're very pleased with how that's going. As a reminder, that study is also powered for endpoints at five years, at 240 weeks, the primary endpoint outcome. We'll be following not just for the one-year histology readout that will lead to filing for accelerated approval, but we'll be following for long-term outcomes. Lastly, the third study is a SYNCHRONY Outcomes, which is an F4 compensated cirrhotics. That is a randomized double-blind placebo-controlled study looking at one dose, not two, of EFX, just the 50 milligram dose. The primary endpoint for biopsy will be at two years, like the data we'll soon see. That is the outcomes portion of it. The clinical events that we're looking at, the hepatic clinical events, will be followed for approximately 260 weeks, roughly five years. And there are key secondary endpoints that are listed here. But with that, I'll probably stop and thank you for your attention. Okay, great. Do we have time for some questions? And if folks have any, just raise your hand and we'll get a mic over to you. But actually, we have a question submitted via the portal, so I think I might start there. And this is sort of a mechanical question related to the mechanics of the 96-week readout coming with the Symmetry trial. Do pathologists reread baseline biopsies, right, both baseline and 36-week biopsies as part of the 96-week assessment? Is there any potential for sequence bias? And do you use the same two to three pathologists in scoring histologic change? Okay, so that's a multi-layer question. So let me just go backwards. The ones I can remember, you'll remind me on the portions I'll forget. So the number of pathologists is the same. So there are three pathologists. We follow the same practice that we have in the Harmony study. That is that two pathologists have to come to consensus. And if they can't come to consensus, the third will serve as an adjudicator. But really, this study is mostly read by two pathologists. And the second question, or maybe the first part of the question, was, as I believe, about sequence bias. So we address sequence bias by inserting random slides that sort of are screening biopsies that are done throughout. So as they're reading, they reread some original screening samples that may not be patients who are actively in the study, but they can't assume that because the patient is later in the trial, that's necessarily a 96-week biopsy. They don't, however, reread the baseline and 36 weeks as part of the study. They're not part of. not part of. We're not rereading those. There are just some samples that are used to address the sequencing issue, but without reassessing the biopsies that had already been read out. Okay. I think that's what the question was. Yep. That seems to speak to it pretty well. Maybe in just the second part of the question, and I'm sure you get this a lot, we certainly do, which is just how to think about the patient retention at the 96-week readout, given that it's likely that these are sicker patients relative to those in the non-cirrhotic patients assessed in the Harmony trial. Yeah, so I think that's a very important, we get that question too. So the patients are sicker. These cirrhotic patients have more advanced liver disease, but they have more advanced everything disease: diabetes, cardiovascular disease. They're just, unfortunately, they face a lot more, the greater number of medical challenges. That being said, the question is really focused on retention. So unlike the pre-cirrhotic patients, for which there, thankfully, is now one approved drug, there are no approved drugs for F4. So while they do face more advanced disease, at the same time, they also, because of the week 36 results, they know that this compound has led to one quarter of patients on the 50 milligram arm being no longer cirrhotic. And that's a pretty compelling reason to stay on the study. There is another reason, which is that, like the Harmony study, the Symmetry patients who are randomized to placebo are offered open-label drug in study 107 as a follow-up and just as a way to balance committing to a placebo in a clinical trial for two years. So it's a reason to stay on the study because there is the opportunity to access open-label drug. Question here. Sorry, a quick one. So in the Symmetry trial, are the patients being followed by non-invasive methods like FibroScan at all, or it's just the biopsies at the week 36 and week 96? They're being followed by both. So they get a biopsy at week 96, but the non-invasives, whether it's ELF score, FibroScan, are continued from week 36 onward. So we will have all of those data week 96. Okay. It'll be a little bit, an additional six weeks, sixty weeks since the 36-week assessment. I guess, what is your expectation around the sort of level of deterioration or fibrosis worsening on the placebo arm, maybe perhaps referencing the existing natural history or clinical data? Is there sort of an expectation that you would have us keep in mind in terms of how the placebo arm may perform with the longer time point? Yeah. So unfortunately, as I shared from that Kaplan-Meier curve, the pace of clinical dysfunction or demise is more rapid for F4 patients. So you saw that at five years, 50% of the patients will. There's a 50% mortality. And so when one thinks of a placebo patient for two years being untreated, one would think the portion of the liver that is F4 would progress. So one thinks, recognizing, and this gets at the false positive sampling, is that say that a patient at baseline is roughly half F4, half F3, it's very unlikely that that ratio would remain the same and be so at two years. And so as a result, the increase in proportion of the liver that is F4, more likely than not, will lead to a likely lower placebo false positive rate at week 96. Now, we don't expect it to be zero, but we'd be surprised if it's the same number or higher. Just on the tolerability profile in the F4 population, and specifically just on the point of bone loss, the potential for bone loss, I mean, yeah, can you just sort of talk about any incremental propensity to experience bone loss in the F4 population relative to the non-cirrhotic population and what would be an acceptable sort of loss margin for still chronic treatment of the cirrhotic population? Yeah. So in the cirrhotic population at week 36, we did see a non-significant difference at the lumbar spine at week 36, and then we did see a significant difference in the hip. That contrasts with the week 48 measure in the non-cirrhotic, which is both reasonable, placebo-like. I think it really speaks to the advanced disease that these patients face, not only in diabetes, liver disease, and as well as bone disease. I think in terms of what the benefit risk is, I think what you're driving at, Eric, I think the benefit risk is very different in this population, primarily because of the mortality as being so acute. I'll ask also is the fact that, unfortunately, many of these patients had osteopenia at baseline, but were untreated with pretty basic measures of standard of care, which are calcium and vitamin D supplementation, as well as existing drugs, anti-resorptive drugs for osteopenia that were not being utilized. So as we go forward, we're highlighting the importance of bone safety for all patients in this study, and that's something we hope to improve upon in phase lll. You highlighted kind of almost a subpopulation to some extent within the cirrhotic population, those with cryptogenic cirrhosis, right, or the kind of burned-out cirrhosis. In Symmetry ITT, it seems like that comprised about 17% of the population. How reflective is that of the sort of real-world prevalence of that subtype? And for your ongoing SYNCHRONY Outcomes trial, how is—I guess, what allowances are there for—what's the expected composition of cryptogenic patients? Is there an enrollment cap or quota there? Yeah. So I think cryptogenic patients are among the most advanced compensated cirrhotic patients that there are. That's why they don't have as much fat because fibrosis has largely sort of moved that out from the hepatocytes. I think there's not great data on what the true, in terms of natural history and what the percentage is. The numbers we've seen are up as many as 15% of the patients. So at 70%, we're a tad higher. In terms of where the study is, we've seen, in terms of our entry criteria, likely to be similar to what we had in Symmetry, probably around 20%. So will we get there? We're not sure. But I think it's important when one thinks about an outcomes-based study, the more advanced patients are those who reach outcomes sooner. So it's important, which is why we included them in phase lll, Phase 2b, is to help us understand how they respond and how they tolerate the drug and how suitable they would be to have in phase lll. Just picking up on the progress update with SYNCHRONY Real-World having fully accrued that trial, kind of a broader eligible patient population, drawing across the non-cirrhotic and cirrhotic spectrum. Just to what extent does sort of the enrollment pace there inform the pace of enrollment of SYNCHRONY Histology? I guess, how is accrual there trended relative to expectations? So I think it's important to note that everyone who was a SYNCHRONY Real- World patient was screened for SYNCHRONY Histology. So the fact that this trial enrolled as rapidly as it has is reflective of the screening pace in SYNCHRONY Histology. So I think when one looks at that, we're pleased with what's happened in SYNCHRONY Real- World. Similarly, we're pleased with where we are with SYNCHRONY Histology. All right. I think we might leave it there for questions. Thanks, everyone, for tuning into the session. Thanks for the presentation, Andrew. Thanks very much for having us.