Thank you for standing by. Welcome to the Akero Reports Data for 16-Week Study in Cirrhotic NASH Patients. I am now handing over to William White, Chief Financial Officer and Head of Corporate Development at Akero Therapeutics. Thank you, and good afternoon. Joining me on the call are Andrew Cheng, President and CEO of Akero, Kitty Yale, Chief Development Officer, and Tim Rolph, Chief Scientific Officer. Today, we will be sharing 16-week results from the expansion cohort, known as Cohort C, of our BALANCED phase IIa clinical study of efruxifermin, or EFX, for the treatment of NASH. Before we begin, I'd like to remind you that various statements that we may make during the call will include forward-looking statements as defined under applicable securities laws. Forward-looking statements include those regarding implications of this analysis of Cohort C of the BALANCED study, our future plans, including our plans around the development of EFX, prospects and strategy, the potential impact of COVID-19, financial goals and guidance, product attributes and pipeline, drivers of growth, and other statements that are not historical fact. Management's assumptions, expectations, and opinions reflected in these forward-looking statements are subject to risks and uncertainties that may cause actual results and/or performance to differ materially from any future results, performance, or achievements discussed in or implied by such forward-looking statements. The company can give no assurance they will prove to be correct and will not provide any further guidance or updates on our performance during the quarter unless we do so in a public forum. Please refer to the press release we issued today and risk factors included in the company's filings with the Securities and Exchange Commission for a discussion of important factors that may cause actual events or results to differ materially from those contained in our forward-looking statements. Prior to this call, we issued a press release regarding data for our phase IIa BALANCED study, which is available on our website at akerotx.com under Press Releases in the Investor Relations section. We also prepared a presentation, which we will reference during our remarks. This presentation will be available on our website under Events and Presentations in the Investor Relations section of our website. I will now turn the call over to Andrew Cheng, Akero's President and CEO. Thank you, Bill, and thanks to all who have joined today's webcast. Today marks an important new milestone for Akero Therapeutics. We reported exciting new data from an expansion cohort of our phase IIa BALANCED study in NASH patients, or Cohort C, which evaluated efruxifermin, or EFX, in the treatment of cirrhotic NASH patients with compensated disease. Most importantly, we reported that 33% of EFX patients achieved fibrosis improvement without worsening of NASH, and 25% achieved NASH resolution, in each case compared to 0% for placebo. These encouraging results pave the way for us to expand EFX development into cirrhotic NASH patients, a group with the highest unmet medical need. On slide three, we review the strong foundation on which today's results are based. That foundation begins with our molecule, which we believe represents Amgen's innovation in protein engineering, an Fc fusion protein designed based on their Enbrel scaffold. EFX incorporates a modified sequence of human FGF21 with two point mutations that prevent degradation. As a result, extending half-life to three to four days, which supports once-weekly dosing. Based on clinical observations, as well as in vitro pharmacology, we believe EFX's unique engineering delivers balanced potency across FGF21's receptors comparable to native human FGF21. Last year, we reported results for EFX in patients with NASH and F1 through F3 fibrosis. As shown on the right-hand side of the slide, these data show EFX's potential to address all core facets of NASH with improvements in histology, including both fibrosis improvement and NASH resolution, as well as liver fat, ELF score, and PRO-C3, ALT and AST, lipoproteins, hemoglobin A1c, and weight loss. Most notable among these improvements was 2-stage reversal of fibrosis in 11 of 22, or 50%, of F2 and F3 patients. This magnitude of resolution of fibrosis after only 16 weeks of treatment suggests two distinct pathways are involved in EFX's therapeutic action. One, a metabolic effect that reduces steatosis and dampens hepatocyte stress, in effect exerting an indirect anti-fibrotic effect. The other, a direct anti-fibrotic effect. Before we dive further into the data, it's important to underscore that cirrhotic patients represent a distinct patient population, separate from the F2 and F3 population that is projected to be 11 million in 2030. As shown on slide four, FDA has issued draft guidance specific to F4 patients, a population projected to be 3.5 million Americans by 2030. As explained by FDA in its guidance, the treatment goals for cirrhotic patients differ from patients with less advanced fibrosis. The goals of treatment for compensated NASH cirrhosis are to halt or slow progression of fibrosis, prevent clinical decompensation, and reduce the need for liver transplantation and improve survival. Slide five illustrates the poor prognosis of cirrhotic patients and shows why reversing fibrosis and improving survival should be the main objective for this patient population. Fibrosis stage, but no other histologic features has been associated independently with increased mortality, transplantation, and liver-related events. The Kaplan-Meier plot on the right demonstrates how liver-related mortality increases dramatically from F3 to F4 fibrosis, with approximately 60% of F4 patients dying within five years absent a liver transplant. This means the risk of liver failure and hepatocellular carcinoma, as well as the need for liver transplantation, is substantially higher for cirrhotic patients. Slide six highlights data presented by Dr. Arun Sanyal at AASLD 2020, showing that reversal of cirrhosis was associated with greatly improved clinical outcomes for NASH patients. The charts represent pooled analysis of Gilead studies with selonsertib and simtuzumab in patients with F4 cirrhotic NASH. The incidence of liver-related clinical events for the pool of patients, whether treated or placebo, with reversal of cirrhosis, shown in the green bars, was compared with that with a pool of patients who remained cirrhotic, shown in the red bars. This analysis illustrates a reduction of greater than 80% in risk of liver-related clinical events associated with reversal of cirrhosis, emphasizing the medical need and benefit to be gained. As illustrated on slide seven, there have been several attempts to be the first investigational product to show success in cirrhotic NASH patients. Here we show each of the investigational products that have been evaluated as a single agent in cirrhotic NASH patients for which fibrosis improvement or fibrosis improvement without worsening of NASH have been publicly reported. Unfortunately, none have succeeded, even when dosed for one to two years. I'll turn the presentation over to our Chief Development Officer, Kitty Yale, to explain why our confidence in EFX's potential for treating chronic cirrhotic patients is high. Thank you, Andrew, good afternoon, everyone. I'm pleased to report our end of treatment results from Cohort C, the extension to our phase IIa BALANCED study in patients with compensated cirrhosis fibrosis Stage 4. Before sharing the results, I'd like to review the study design for Cohort C, which is shown in slide eight. The study was a randomized, double-blind, placebo-controlled study. All patients had biopsy-confirmed NASH F4 as read by a local pathologist. The study enrolled 30 patients in a two to one randomization, with 20 patients in the EFX 50 mg arm and 10 patients in placebo. Patients were randomized to receive once-weekly subcutaneous doses of EFX or placebo for 16 weeks. The primary endpoint of the study was to assess safety and tolerability of EFX in NASH patients at the greatest risk of progressing to end-stage liver disease. The study was originally designed to have non-invasive efficacy endpoints, specifically liver stiffness by transient elastography using FibroScan and serum markers of fibrosis, PRO-C3 and ELF. However, the protocol was subsequently amended after requests from patients and investigators to add end of treatment biopsies at week 16. These biopsies were patient optional as the amendment was implemented after patients had already consented to the study. Today, we report top-line data on a combination of efficacy and safety endpoints. On slide nine, we review the baseline demographic, which are consistent with what have been reported in other cirrhotic NASH clinical studies and are generally representative of F4 patients. Half of the patients had diabetes. Mean AST and ALT values are in the low 30s, consistent with Stage 4 fibrosis. ELF and PRO-C3 levels are higher than seen in the BALANCED main study. Again, consistent with higher levels of fibrosis. Liver stiffness values, again, are consistent with the cirrhotic population. Mean triglyceride levels are substantially lower than seen in the F1 to F3 patients in the BALANCED main study, as expected because of diminished hepatocyte population in livers of patients with cirrhosis. Patient disposition is shown in slide 10. 30 patients were randomized and dosed. 27 of 30 patient biopsies were confirmed to be F4 by the central reader. The three other patients were not included in the histology analysis set. Two patients discontinued prior to week 16, one placebo patient who withdrew consent and one EFX patient due to adverse events. Eight patients did not consent to end of treatment biopsy. End of treatment biopsies were obtained for 17 confirmed F4 patients, five on placebo and 11 on EFX. Slide 11 summarizes the percentage of patients with fibrosis improvement of 1- stage without worsening of NASH. Fibrosis improvement without worsening of NASH was achieved in 33% of the EFX arm, compared to 0% in the placebo group. An impressive level of response, particularly given the short study duration of just 16 weeks. While not powered to assess the statistical significance of histological endpoints, we are not aware of any other reported results showing this level of fibrosis improvement in patients with compensated cirrhosis. As Andrew described previously, a 1-stage improvement in fibrosis could be expected to translate into a greater than 80% reduction in the relative risk of liver-related clinical events. On slide 12, we report multiple non-invasive markers of fibrosis, which provide support for the histological fibrosis improvement seen with EFX. The chart on the left reports change from baseline in liver stiffness measured by transient elastography. Here we see absolute reduction of 5.7 kilopascals for EFX, compared to a reduction of 1.9 kilopascals for placebo. This is approximately a 26% reduction with EFX, a magnitude that has previously been correlated with a 1-stage improvement in fibrosis. The middle chart reports change from baseline for a serum biomarker of new collagen synthesis in the liver, PRO-C3. Here we see a statistically significant absolute reduction of nine micrograms per liter for EFX, compared to 3.4 for placebo. Approximately a 35% reduction with EFX. The absolute reduction observed for EFX is greater than the reported magnitude of PRO-C3 reduction quoted in the literature as correlating with 1-stage improvement in fibrosis. The right chart reports change from baseline in enhanced liver fibrosis, or ELF score, a non-invasive test derived from an algorithm based on three serum biomarkers of fibrosis. Elevated serum levels of these analytes represent increased turnover of the extracellular matrix and have been shown to correlate with various stages of liver fibrosis and cirrhosis. Here we see a statistically significant reduction of 0.4 for EFX compared to a 0.3 increase for placebo. The magnitude of improvement of serum biomarkers of fibrosis in this F4 cohort is comparable to what is observed in the F1 to F3 population in the main portion of the BALANCED study and confirms the potential for reproducible and robust effects of EFX on fibrosis. Slide 13 shows our other histological endpoint, NASH resolution, which was achieved in 25% of EFX patients compared to 0% in the placebo group. To note, there was no overlap between patients achieving fibrosis improvement and NASH resolution. As a result, a total of 7 out of 12 EFX patients in the biopsy analysis set, or 58%, met either fibrosis improvement or NASH resolution. We believe that reducing steatohepatitis, as indicated by NASH resolution, should ultimately, in time, lead to reversal of fibrosis. On slide 14, we report changes to the markers of liver injury, both ALT and AST. As highlighted earlier, patients in Cohort C had lower liver enzymes at baseline, a mean of 32 and 30 for ALT and AST respectively, consistent with the smaller hepatocyte population in livers of patients with cirrhosis. For reference, baseline ALT ranged from 51-63, and AST ranged from 35-45 amongst F1 to F3 patients in the main portion of the BALANCED study. The left chart reports change from baseline in ALT, and here we see a statistically significant absolute reduction of 10 units for EFX compared to 1.3 for placebo. Approximately a 30% reduction. The right chart reports change from baseline in AST. Here again, we see a statistically significant absolute reduction of 9.6 units for EFX compared to 4.5 for placebo. Again, approximately a 30% reduction. Let's shift now to safety and tolerability, beginning with a high-level overview on slide 15. In terms of discontinuations, one placebo patient withdrew consent, and one patient in the EFX arm discontinued due to adverse events. This patient experienced abdominal distension, constipation, diarrhea, and pruritus, discontinuing treatment at week five. One patient in the placebo arm reported a serious adverse event of pulmonary embolism. Slide 16 provides an overview of the most frequently reported drug-related treatment emergent adverse events. The most frequent events were transient, mild to moderate diarrhea and nausea, which often resolved on study without treatment. All of the injection site reactions were Grade 1, and there were no reports of tremor. I'll now have our Chief Scientific Officer, Timothy Rolph, present our lipoprotein and glycemic control data. Thank you, Kitty, and good afternoon, everyone. By way of context for Slide 17, more than 80% of NASH patients are dyslipidemic, with elevated levels of triglycerides and LDL cholesterol and low levels of HDL cholesterol. Dyslipidemia is a major contributor to high incidence of cardiovascular morbidity and mortality amongst NASH patients. As with the BALANCED main study, clinically meaningful improvements in lipoprotein profile are evident following 16 weeks of treatment with EFX. Starting on the left, levels of triglyceride were reduced 29% by comparison to an increase of 1% for placebo. This reduction in triglyceride is not as large as was observed in prior EFX trials. However, mean levels at baseline were 135 mg per deciliter, considerably lower than the corresponding value of approximately 180 mg per deciliter in the BALANCED main study. Moving to the right, LDL cholesterol was reduced significantly by 8%, compared with a 16% increase for placebo. The next chart shows a substantial increase in HDL of 33%, compared with 3% for placebo, in line with prior studies with EFX in NASH and type 2 diabetes patients. The final chart shows change from baseline in non-HDL cholesterol. Because EFX reduces cholesterol primarily by decreasing the VLDL, with a smaller effect on LDL, the potential of EFX to lower bad cholesterol is best captured by change in non-HDL cholesterol. Like LDL cholesterol, non-HDL cholesterol is a causal risk factor for cardiovascular disease. Levels of non-HDL cholesterol were reduced significantly by 14%, compared with a 12% increase for placebo. To put Slide 18 in context, approximately half of F4 NASH patients have type 2 diabetes. Generally, their diabetes is not well controlled, so improving their glycemic control is highly desirable. As seen here, EFX elicited clinically meaningful improvements in multiple markers of glycemic control, which we believe can be attributed to insulin sensitization. Starting from the left, hemoglobin A1c is a clinical diagnostic for long-term control of blood glucose. Hemoglobin A1c was reduced significantly by 0.4% absolute after 16 weeks treatment, compared with an increase of 0.1% for placebo, an improvement consistent with that observed in the BALANCED main study. The next chart shows change from baseline in adiponectin, generally accepted as a biomarker of insulin sensitivity. Here, we see a highly significant mean increase of 95% for efruxifermin-treated patients, compared with an increase of 4% for placebo. Again, comparable to the BALANCED main study. The next histogram shows change from baseline in C-peptide, the best indicator of insulin secretion. A significant reduction of 20% was observed for treated patients, indicating lower rates of insulin secretion. This contrasts with a smaller decrease of 7% for placebo. Achieving better glycemic control by improving insulin sensitization is highly desirable because it's rectifying the fundamental driver of type 2 diabetes, that is insulin resistance. This means EFX has a potential to achieve a sustained reduction in hemoglobin A1c, in contrast to diabetes therapies which promote insulin secretion, whose efficacy wanes over time. Improved glycemic control and restoration of a healthy lipoprotein profile have now been observed in three independent studies with efruxifermin. Amgen's original phase I study in type 2 diabetes, BALANCED main study in F1, F3 NASH, and now Cohort C in F4 NASH, underscoring the reproducibility of these beneficial effects. The final chart shows body weight change after 16 weeks treatment. As observed in the BALANCED main study, there is a trend to lose weight, approximately 4 pounds-5 pounds, while the placebo group trended up by about 2 pounds. This consistent trend toward weight loss contrasts with another class of insulin sensitizer, the PPAR-gamma agonists. This class includes established antidiabetic drugs like pioglitazone, whose use has declined substantially because of weight gain and edema, and lanifibranor, for which encouraging efficacy results in NASH nonetheless associated with weight gain of about 5 pounds-6 pounds and an incidence of 6%- 8% edema. We continue to view the trend toward weight loss observed with EFX as a key element of differentiation, with the potential for weight loss likely to be attractive to NASH patients and clinicians. These very encouraging metabolic data should be viewed holistically rather than in isolation. We believe these results support the potential for EFX to rectify each aspect of the metabolic dysfunction associated with NASH. As seen in the BALANCED main study, it has improved glycemic control by enhancing insulin sensitivity, restored a healthy lipoprotein profile, and helped lower body weight. Last summer, we said that these broadly based improvements increased our confidence that the rapid reduction of steatohepatitis and collagen deposition seen in BALANCED would be sustained, in turn, allowing further resolution of fibrosis beyond the highly encouraging improvements evident after just 16 weeks of treatment. The magnitude of metabolic improvements also points to the potential of EFX to reduce the high incidence of heart attack and stroke among NASH patients. Today's results strengthen our confidence. The breadth of desirable effects elicited by EFX sets it apart from other candidates in development for NASH, which frequently trade off resolution of liver pathology against undesirable effects on lipoproteins, increased body weight, and no improvement in glycemic control. By restoring a healthy metabolic profile to the whole body, EFX appears to reduce the excessive metabolic load on the liver of patients with NASH. The results are consistent with our predictions based on FGF21 biology and efruxifermin's engineering. Nevertheless, these results again exceeded our expectations and support further development for this population. On slide 19, we show EFX's potential to reverse fibrosis without worsening NASH by comparison with results of prior studies, which Andrew summarized earlier. Acknowledging these are not head-to-head comparisons and employ different study designs, albeit with comparable F4 patient populations. The improvement in fibrosis observed in 33% of treated patients after only 16 weeks of treatment with EFX is double the highest response reported for any other single development candidate and twice the highest response for a placebo, when all of these compounds were dosed for a period of roughly one to two years. On slide 20, we offer an interpretation of these exciting results. We know it's possible to reverse fibrosis by reducing or eliminating the underlying pathogenic drivers of steatosis and hepatocyte stress. This allows the hepatocyte population of liver to regenerate, but this takes time, a commodity in short supply for F4 patients. We believe it certainly takes longer than 16 weeks because fibrosis is so extensive in cirrhotic liver. As highlighted earlier, our BALANCED data suggests that EFX exerts both direct and indirect antifibrotic effects. Today's results, we believe, provide further evidence of EFX's direct antifibrotic effects, as suggested by the preclinical literature on FGF21. We believe the critical question in NASH development is whether a compound has the potential to act directly or merely indirectly to reverse fibrosis. We believe today's results provide the strongest evidence yet of EFX's direct antifibrotic properties. The reversal of fibrosis by 1- stage in 33% of cirrhotic patients and 2-stage improvement of fibrosis in F2, F3 patients, in each case after only 16 weeks of treatment, likely reflects direct antifibrotic activity. There likely isn't enough time for acting only on underlying disease drivers to yield these kinds of results in 16 weeks. Recall that most early NASH studies were 18 months or longer because it was believed it would take that long to see whether there was a discernible impact on fibrosis. When one thinks about the roughly 60% five-year mortality rate for cirrhotic patients Andrew presented earlier, it's easy to see how fibrosis reversal is especially advantageous for cirrhotic patients. There remains an important role for indirect antifibrotic activity. Addressing underlying NASH disease drivers may indirectly contribute to fibrosis reversal from F1 to F3 patients who have longer time for the liver to regenerate. Most importantly, redress of the underlying NASH disease drivers is necessary to sustain fibrosis reversal across all stages of fibrosis, whether F1 through to F4. That's why we believe EFX has so much potential. From what we have seen in our clinical trials to date, we believe EFX may offer the complete package. It has addressed the underlying disease drivers by reducing liver fat and hepatocyte stress, which can help reverse fibrosis over time and preserve fibrosis reversal. EFX also appears to have the horsepower to reverse fibrosis by acting directly to reduce inflammation and collagen synthesis. I'll now hand the presentation back to Andrew. Thank you, Tim. Let me conclude with a quick review of where we are in EFX development with slide 21. On the left-hand side of the table, we provide an overview of our phase IIa program, consisting of the BALANCED main study in F1-F3 patients and Cohort C in F4 patients. The right-hand side of the table shows what we plan to undertake in two phase IIb studies in parallel in two distinct NASH populations, F2 and F3, and F4. Earlier this year, we announced initiation of our phase IIb HARMONY study in F2, F3 patients. That study is evaluating 28 and 50 milligram doses for a 24-week treatment period. We expect to report HARMONY results in the second half of 2022. We are still in the process of designing our planned phase IIb F4 SYMMETRY trial. Subject to review by regulatory authorities, we plan to initiate SYMMETRY in the second half of 2021. Details of the SYMMETRY trial design will be reported later this year. We look forward to working with the FDA and EMA to further our development program and ultimately, if approved, to making an exciting new treatment available to patients. Let me take a moment to extend a heartfelt thank you to all of the patients, investigators, and study site staff who participated in the BALANCED study. Today's exciting data would not have been possible were it not for our patients, many of whom completed clinic visits and study procedures despite the ongoing COVID-19 pandemic, and the dedication of our investigators and their teams, all of whom work tirelessly to serve their patients despite the challenges of the global pandemic. We are truly grateful for their commitment during these difficult times. I'd now like to turn things over to the operator for questions and answers. Thank you. First question comes from Eric Joseph with JP Morgan. Good afternoon. Congrats on the data, thanks for taking the questions. We have a couple. First, with respect to the data on NASH resolution, can you comment a bit on sort of average NASH scores that were observed at baseline in the two arms and how they trended over the treatment period? Secondly, were there any notable baseline patterns among EFX-treated patients who didn't see a 1-stage reversal in their fibrosis? Did perhaps gender play a role, would you anticipate a greater proportion of subjects achieving that threshold with longer time on drug based on some of the non-invasive analyses and biomarker analyses you're conducting? Just thirdly, as a market sizing question, of that 3.5 million projected estimate of cirrhotic patients or cirrhotic NASH subjects, what proportion is reflected by the patient eligibility criteria in Cohort C? Would you anticipate a similar benefit risk profile in subjects with somewhat more advanced disease, perhaps those with portal hypertension or variceal lesions? Thanks for taking the questions. Thank you, Eric. Three questions are tricky, let me just start with the last one since that's easiest for me to remember. I think in terms of the entry criteria, we developed them pretty broadly so they would be generalizable to patients with Child-Pugh class A compensated cirrhosis. For patients with more advanced disease, I think we haven't studied them, so we'll have to wait until we get more data as we look to future studies, and we may expand our entry criteria to address those. When you think about the three and a half million in 2030, difficult to see how people will break down in terms of Child-Pugh A, B, and C, as one thinks about that overall. In terms of your other first two questions, they're pretty specific. I would say that we're at a top-line data phase. We haven't been able to generate those data that would answer your question at this time. Okay, great. Well, congrats again. Thanks for taking the question. Thank you, Eric. Our next question is from Matthew Harrison with Morgan Stanley. Great. Good afternoon. Thanks for all the detail and thanks for taking the questions. Two from me. First one, Andrew, is would you expect, and I know you sort of answered this on the last question, but when we think about F4 patients versus other patients who aren't as severe, would you expect to continue to see a greater benefit over time in these patients, or is there anything specific to the patient characteristics that you wouldn't expect to see that same trend that you've seen in earlier line patients? I guess the second question is just really about how you think about, I guess what I should ask is, what do you think might be the regulatory hurdle here for an F4 population, just given that no one else has tried to pursue that? I realize, it's under review, and you're discussing it still, but, just broadly, what are your thoughts on what the regulatory hurdle might be? Thank you, Matthew. Let me do the first one, and I'll ask Kitty to do the regulatory one. Overall, I would say that when we think about these patients, we obviously have the four patients that had a 1-stage improvement of fibrosis already. When we begin to look at the patients that had NASH resolution, those are the types of patients we begin to see that where there's both an indirect and direct component playing a role there. Those who are beginning to resolve their inflammation and ballooning, we feel are on their way towards improvements in fibrosis. As we begin to think of the seven of the 12 patients who had one form of histologic improvement or the other, it gives us a little bit of a preview for what we could see down the road with longer-term dosing, recognizing that 16 weeks is incredibly short. We think that what we're seeing here really is the floor of what we can achieve, not the ceiling. We're looking forward to demonstrating that in future studies. Let me turn it over to Kitty now to comment on the regulatory pathway. Hi. I'm sure you're aware that the current regulatory guidelines for compensated cirrhotic patients are looking for endpoints in terms of clinical outcomes versus histologic. When you read that particular guidance document, the draft guidance, it's very clear that the FDA, perhaps based on the lack of positive data in cirrhotic patients, are really concerned that maybe fibrosis reversal is not possible in this patient population. I think, with all regulatory guidance, new data will help influence the regulators. I think it's really up to us now to share our data and then to really sort of discuss with the regulators the best way for us to move EFX forward. I think we would still look at a combination of histologic and clinical outcomes in any F4 patient study that we would do, because based on the data Andrew presented earlier today, there really is clear benefit in terms of clinical outcomes by regressing fibrosis by Stage 1. Thank you. Our next question comes from Monica Mirchandani from Evercore. Great. Thanks for taking the questions. Congrats on the update. Just had two questions from our end. The first is, as we think about histology here, were there any meaningful differences in benefits in the non-invasive metrics between patients who elected to do a post-treatment biopsy and those who didn't? Then I just wanted to follow up on the previous question. Did you look at the time course of benefit for some of these non-invasive markers of fibrosis, especially as we think about extrapolating benefit to a longer study and what you see there? Thank you. Hi, Monica. Let me ask Kitty to answer your question about how consistent the response was in the non-invasive measures, recognizing that we didn't get biopsies in every one. Yeah. Hi, Monica. The results were pretty consistent across the board for patients that had both histology and end of treatment biopsies and those that did not. We haven't done a full correlation of each individual patient, but basically, on looking at the data, there's really nothing distinct that I can really see about the patients that had biopsies versus not. Maybe in regard to your second question, we do have data that will show the response over time. We don't have that data to present currently right now, and that's something we will present at a future upcoming scientific conference. Does that answer your question? Yeah. Thank you. Thank you. We have time for just one more question. Question from Ed Arce with H.C. Wainwright. Hi, good afternoon, everyone. This is Thomas asking a couple questions for Ed. Also want to say congratulations on the great results in these patients, and thank you for the questions. Perhaps, switching gears to adverse events and that single patient who discontinued the study. Would you say it's earlier on in the study or later in the study over 16 weeks? Also, second question, is there an expansion study for patients who completed treatment in this Cohort C? Hi, Thomas. It's Andrew. I would say for the second question, we do not have an extension cohort for this study on patients who completed Cohort C. At the time we designed this, we only had coverage for 16 weeks of tox, so we had to stop the study at that time. Maybe ask Kitty to talk a little bit, at a high level, about when this patient discontinued. This patient actually discontinued at week five. Had four previous doses of EFX before they discontinued, so they completed the first month of treatment. In general, the adverse events, you mentioned this, generally mild, but are they in general earlier in the study or later in the study? Yeah. In general, yes, the GI adverse events were mild to moderate and sort of transient or intermittent in nature. It is interesting, when I was asking some of the investigators to describe the diarrhea, I basically heard them really describe it as sort of non-urgent. It's not like these patients are running to the bathroom and therefore really not affecting day-to-day activities and more sort of the frequency of loose stools. Okay, understood. Thank you so much for the details and congratulations again. Thank you, Thomas. I think, operator, we're sort of out of time. Operator, I think we have time. We have one more question available from Michael Yee from Jefferies. Go ahead. Oh, okay. Hey, guys. Yeah, not sure what's going on there. Maybe actually if I take a step back, you sort of talked about it, but my question was around the idea that you had a number of people who had a fibrosis improvement and a number of people who had a NASH resolution improvement, but neither overlapped. Is your view that actually the NASH resolution people eventually would become a fibrosis improvement if there just is more time, and so the learnings here are that in F4 patients, it's a little bit different than F2/F3, and just with more time, these results could actually get a lot better? Is that sort of the thinking? Tie that together with the learnings overall about this drug. Is your view that this drug ultimately should have similar fibrosis improvements, 40%-50%+ in both populations? Thank you. Hi, Mike, it's Andrew. I would say the first part of the question is yes. I think it's important to recognize that there's some heterogeneity when it comes to the amount of steatosis in some of these F4 patients. Some have more, some have less, and those who that have less, it's a little more difficult for one thinks about the indirect pathway where people are getting reductions in steatosis leading to improvements in hepatocyte stress, and then ultimately improvements of fibrosis. We think for those patients that have NASH resolution, they're likely to lead to fibrosis improvements. Not all the patients have enough liver fat remaining because it's been replaced by fibrous tissue to benefit from that pathway. In terms of longer-term dosing, we see this compound having the potential to have high levels of histologic improvement when it comes to 1-stage improvement of fibrosis. I think we agree with you. Great. Thank you. Thank you. This concludes our conference for today. Thank you for your participation, ladies and gentlemen. Have a good night. You may now disconnect.