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Overview

TL;DR — MASLD is hepatic steatosis in the presence of at least one of five cardiometabolic criteria, renamed from NAFLD in June 2023 by a 236-panellist multisociety Delphi process (Rinella 2023, PMID 37363821). It affects roughly 30% of the world's adults (Younossi 2023, PMID 36626630; Riazi 2022, PMID 35798021), rising toward 41.4% of US adults by 2050 in modelling (Le 2025, PMID 39821400). Four facts organise everything else. First, fibrosis stage is what predicts outcome — no other histological feature does, and a histological diagnosis of steatohepatitis adds essentially nothing once fibrosis is known (Angulo 2015, PMID 25935633; Hagström 2017, PMID 28803953; Akbari 2024, PMID 38293684). Second, most people with MASLD die of something other than liver disease — cardiac deaths outnumber liver deaths about 4.5:1 in unselected cohorts (PMID 36626630), though the ordering inverts at advanced fibrosis. Third, after two decades of failure, two drugs were conditionally approved in eighteen months — resmetirom in March 2024 and semaglutide in August 2025, both for non-cirrhotic MASH with F2–F3 fibrosis, and both on histological surrogates whose outcome confirmation is still running (Keam 2024, PMID 38771485; Bansal 2026, PMID 41201884). Fourth, non-invasive tests are now operational first-line tools for staging and prognosis and can match or outperform histology in prognostic cohorts (Mózes 2023, PMID 37290471; Aceituno 2026, PMID 41212130). The dominant unresolved tension is that the endpoint licensing the drugs is not the variable predicting the outcome.

What the disease is

Hepatic steatosis (≥5% of hepatocytes) plus at least one of: BMI ≥25 kg/m² (≥23 Asian) or raised waist circumference; dysglycaemia or type 2 diabetes; blood pressure ≥130/85 or treatment; triglycerides ≥1.70 mmol/L or treatment; HDL ≤1.0 mmol/L (M) / ≤1.3 (F) or treatment — in a person drinking less than 140 g/week (women) or 210 g/week (men) of alcohol, with no other cause of steatosis (Rinella 2023, PMID 37363821; Tilg 2026, PMID 41212550).

Above those alcohol thresholds and below the alcohol-related-liver-disease floor lies MetALD; with steatosis but no metabolic criterion and no known cause, cryptogenic SLD. All sit under the umbrella term steatotic liver disease. The full account, including why MASLD and NAFLD overlap by ≥94% but are not identical, is in nomenclature and definitions.

A search rule follows from the rename, and it binds every page here. The literature is split across NAFLD/NASH, MAFLD and MASLD/MASH vocabularies. On 2026-09-02, the union query (MASLD OR NAFLD OR MASH OR NASH OR "steatotic liver disease") returned 78,992 PubMed records against 50,200 for the new name alone. Every search behind these pages unions both vocabularies, and where a cited study enrolled under NAFLD/NASH criteria the page says so.

The disease in numbers

Quantity Value Source
Global adult prevalence 30.05% (95% CI 27.88–32.32) Younossi 2023, PMID 36626630
…alternative estimates 32.4% (29.9–34.9); 29.8% (28.6–31.1); 30.2% (28.7–31.7) PMIDs: 35798021, 34890795, 39094335
Prevalence in type 2 diabetes 65.33% (62.35–68.18) Younossi 2024, PMID 38521116
Prevalence in obesity 75.27% (70.90–79.18) Quek 2023, PMID 36400097
Lean fraction of the MASLD population 19.2% (15.9–23.0) Ye 2020, PMID 32413340
Advanced fibrosis in the general population 3.3% (2.4–4.2) Zamani 2025, PMID 39209202
Cirrhosis in the general population 1.3% (0.9–1.7) PMID 39209202
Progression to cirrhosis 3–5% of patients, usually >20 years Hagström 2024, PMID 39243773
Fibrosis progression from F0 0.07 stages/yr in MASL, 0.14 in MASH Singh 2015, PMID 24768810
Spontaneous fibrosis regression, paired biopsies 22.3% PMID 24768810
All-cause mortality 12.60 per 1,000 person-years PMID 36626630
…of which cardiac / extrahepatic cancer / liver 4.20 / 2.83 / 0.92 per 1,000 PY PMID 36626630
Median survival from first decompensation 2.0 years Noureddin 2024, PMID 38571305

The four organising facts

1. Fibrosis, and only fibrosis

In the multinational NASH CRN cohort of 619 patients followed a median 12.6 years, fibrosis stage — and no other histological feature — was independently associated with death, transplantation and liver-related events; hazard ratios versus F0 were 1.88 at F1 rising to 10.9 at F4 (Angulo 2015, PMID 25935633). In 646 Swedish biopsy patients followed a mean 20 years, hazard ratios for severe liver disease ranged from 1.9 at F0 to 104.9 at F4, and adding NASH to the model improved prediction at no stage (Hagström 2017, PMID 28803953). Liver-related mortality rises roughly exponentially with stage: mortality rate ratio 9.57 at F2, 16.69 at F3, 42.30 at F4 (Dulai 2017, PMID 28130788). Detail in natural history and fibrosis progression.

2. The deaths are mostly not hepatic

Cardiovascular disease is the leading cause of death in the general MASLD population (Duell 2022, PMID 35418240), with pooled cardiovascular event risk HR 1.45 (1.31–1.61) rising to 2.50 (1.68–3.72) with advanced fibrosis (Mantovani 2021, PMID 34555346). Extrahepatic cancer risk rises 1.2–2-fold by site (Mantovani 2022, PMID 33685968) and incident chronic kidney disease 1.43-fold (Mantovani 2022, PMID 33303564). In biopsy-confirmed cohorts the ordering shifts: extrahepatic cancer (aHR 2.16) and cirrhosis (aHR 18.15) dominate the excess mortality (Simon 2021, PMID 33037056). See cardiovascular and extrahepatic outcomes.

3. Two drugs, both conditional

Drug Approved Indication Pivotal result
Resmetirom (THR-β agonist) March 2024, accelerated non-cirrhotic MASH, F2–F3 MASH resolution 25.9%/29.9% vs 9.7%; fibrosis improvement 24.2%/25.9% vs 14.2% (Harrison 2024, PMID 38324483)
Semaglutide 2.4 mg (GLP-1) August 2025, accelerated MASH, F2–F3 Resolution 62.9% vs 34.3%; fibrosis improvement 36.8% vs 22.4% (Sanyal 2025, PMID 40305708)

The placebo arms differ by a factor of 3.5 between these two trials, so the drugs cannot be ranked against each other from published data. Both approvals are conditional on outcome phases still running (clinical trials landscape). Neither is approved in cirrhosis, where every randomised trial to date has failed (cirrhosis and decompensation). Behind them sits a large pipeline of FGF21 analogues, incretin multi-agonists and, distinctively, genotype-directed silencers of PNPLA3 and HSD17B13 (genetics).

Lifestyle remains the largest effect at the top of the dose–response: ≥10% weight loss produced NASH resolution in 90% and fibrosis regression in 45% — in the 30% of a supervised cohort who achieved it (lifestyle and weight loss; Vilar-Gomez 2015, PMID 25865049). Metabolic surgery achieved 84% resolution at five years with progressive fibrosis regression and has a dedicated observational analysis of major adverse liver outcomes (bariatric and metabolic surgery; Lassailly 2020, PMID 32553765; Aminian 2021, PMID 34762106).

4. Biopsy has been displaced

Non-invasive tests can match or outperform histology for predicting clinical events in selected cohorts: 5-year time-dependent AUC 0.76 for liver stiffness versus 0.72 for histology (Mózes 2023, PMID 37290471), and in F3–F4 patients the ANTICIPATE-NASH models achieved C statistic 0.93 versus 0.67 for histological stage (Aceituno 2026, PMID 41212130). The operative pathway everywhere is sequential — FIB-4 first, elastography or ELF second — with biopsy reserved for discordance and competing diagnoses (noninvasive assessment, guidelines). Biopsy retains a role in trials, where it remains the regulatory reference standard despite inter-rater κ of 0.45–0.56 for the inflammatory features that define steatohepatitis (histology and biopsy; Kleiner 2005, PMID 15915461).

5. The category itself is unstable — in two directions

The four facts above are robust. A fifth is newer and cuts underneath them, and it belongs at overview level because it conditions how the rest should be read.

The MASLD label can be contaminated by alcohol. In a prospective at-risk cohort of 2,924 people, 39.0% of those classified as MASLD by self-reported intake had phosphatidylethanol concentrations in the MetALD or ALD range, with under-reporting in 39.5% of the alcohol-recruited group and 11.1% of the metabolically-recruited group, and essentially no over-reporting (Torp 2025, PMID 40945520). If similarly one-directional misclassification occurs in outcome cohorts, it would tend to attenuate MASLD-versus-MetALD hepatic hazard differences; this single at-risk cohort does not establish the size of that bias elsewhere (nomenclature and definitions).

It may also be more than one disease. Unsupervised clustering on six routine clinical variables, validated across three biopsy cohorts and UK Biobank, separates a genetically-linked liver-specific type — rapid hepatic progression, limited cardiovascular risk — from a cardiometabolic type with the same baseline liver phenotype but higher cardiovascular and diabetes risk, each with distinct liver transcriptomes and plasma metabolomes (Raverdy 2024, PMID 39653777). If that holds, fact 2 above (deaths are mostly not hepatic) is a population average concealing two opposite risk profiles.

And the excess mortality may not belong to the liver at all. When the comparator is restricted to people who also carry a cardiometabolic risk factor — the only fair comparison, since cardiometabolic dysfunction is now part of the definition — MASLD was null for all-cause (aHR 1.04, 0.95–1.14), cardiovascular and cancer mortality across 26.7 years of NHANES III follow-up, while MetALD was not (all-cause aHR 1.41, 1.05–1.89; liver 15.04, 2.96–76.35) (Kwak 2025, PMID 38739848). Every other mortality cohort cited on these pages compares MASLD against unmatched controls. The stage-specific hepatic gradients (natural history) are unaffected; what is in question is whether unstaged MASLD carries mortality risk beyond the metabolic dysfunction that defines it.

Mechanism, in one paragraph

Stable-isotope tracing in NAFLD patients apportions hepatic triglyceride to serum non-esterified fatty acids (59.0% ± 9.9%), de novo lipogenesis (26.1% ± 6.7%) and diet (14.9% ± 7.0%) (Donnelly 2005, PMID 15864352). Triglyceride itself is not toxic; specific species — saturated free fatty acids, free cholesterol, lysophosphatidylcholine, ceramides — drive ER stress, mitochondrial dysfunction and cell death (Marra 2018, PMID 29154964). Hepatic mitochondria adapt in obesity (4.3–5.0-fold higher maximal respiration) and fail at the steatohepatitis transition (31–40% lower, with oxidative damage) (Koliaki 2015, PMID 25955209). Injured hepatocytes, recruited macrophages and hepatic stellate cells then form a self-reinforcing fibrogenic network with reactivated developmental signalling (Schwabe 2020, PMID 32044315). The "two-hit" model is obsolete; multiple parallel hits act on a genetically predisposed host (Buzzetti 2016, PMID 26823198). Full account in pathogenesis.

Genetics is unusually tractable: heritability of steatosis 0.52 (0.31–0.73) and of fibrosis 0.50 (0.28–0.72) (Loomba 2015, PMID 26299412), with PNPLA3 I148M as the dominant common variant since 2008 (Romeo 2008, PMID 18820647) and HSD17B13 loss of function as the counterweight (Abul-Husn 2018, PMID 29562163). Both are now drug targets.

Map of this condition

Foundations - nomenclature-and-definitions.md — NAFLD → MASLD, MetALD, MAFLD, and the search rule. - epidemiology-and-burden.md — prevalence, incidence, regional variation, projections.

Mechanism - pathogenesis.md — lipid supply and disposal, lipotoxicity, immunity, fibrogenesis. - genetics.md — heritability, PNPLA3, TM6SF2, HSD17B13, polygenic scores, genotype as drug target.

Diagnosis - noninvasive-assessment.md — FIB-4, elastography, ELF, sequential pathways, failure modes. - histology-and-biopsy.md — NAS, SAF/FLIP, reader variability, digital pathology.

Clinical course - natural-history-and-fibrosis-progression.md — stage-specific outcomes, progression and regression. - cirrhosis-and-decompensation.md — cACLD, portal hypertension, transplant. - masld-related-hepatocellular-carcinoma.md — the pre-cirrhotic tumour problem (border page). - cardiovascular-and-extrahepatic-outcomes.md — where the deaths occur. - masld-and-type-2-diabetes.md — the bidirectional relationship and the case-finding venue. - lean-masld.md — the phenotype BMI-anchored screening misses.

Treatment - lifestyle-and-weight-loss.md — the dose–response, and why attainment is the problem. - resmetirom-and-thyromimetics.md — the first approved drug. - glp1-and-incretin-therapy.md — the second, and the multi-agonist field. - bariatric-and-metabolic-surgery.md — the largest histological effect. - other-pharmacotherapy.md — vitamin E, pioglitazone, statins, and the failures.

Reference and frontier - guidelines.md — societies, agreements and disagreements. - clinical-trials-landscape.md — live NCT records and the surrogate-endpoint problem. - red-flags-and-safety-concerns.md — how this disease is missed and mismanaged. - patient-experience-and-advocacy.md — stigma, quality of life, awareness.

Borders. Hepatocellular carcinoma owns the tumour: staging, treatment, transplant criteria. Type 2 diabetes owns glycaemic management. This condition owns the liver disease from steatosis through cirrhosis, and its cardiometabolic context.

Open questions

  • Does unstaged MASLD add mortality risk beyond its own defining criteria? Null against a metabolically matched comparator over 26.7 years (PMID 38739848); positive against unmatched controls in every other cohort. The designs answer different questions and only the first answers the clinical one.
  • Is MASLD one disease? Two data-driven clusters with opposite dominant risks and distinct transcriptomes and metabolomes (PMID 39653777), plus PheWAS evidence for at least seven genetic subtypes (genetics). The 2023 process defined the boundary of the category carefully and did not ask whether the interior is homogeneous.

  • How much of what is called MASLD is alcohol? 39.0% by biomarker in one at-risk cohort (PMID 40945520), unreplicated in a general population and untested against outcomes. The full tiered set is in OPEN-QUESTIONS.md. The four that shape the field:

  • Does histological improvement translate into fewer clinical events? Both approved drugs rest on a surrogate whose validity as a treatment-effect transfer measure has never been demonstrated (Taylor 2020, PMID 32027911). The answer arrives with the outcome phases of MAESTRO-NASH and ESSENCE.

  • Why does the disease's leading cause of death sit outside the specialty that manages it? No care model with cardiovascular risk reduction as the primary managed outcome has been tested.
  • Should genotype enter risk stratification, now that it is also a drug target? It predicts progression, reclassifies indeterminate FIB-4 patients and directs two clinical programmes, and appears in no clinical pathway.
  • Is MASH cirrhosis reachable? Every randomised trial in compensated MASH cirrhosis has missed its primary endpoint, and it is the stage where the events are.

Every page above. Start with nomenclature and definitions if the vocabulary is unfamiliar, natural history and fibrosis progression if you want the prognostic core, or clinical trials landscape if you want the frontier.

References

  1. Rinella ME, Lazarus JV, Ratziu V, et al. A multisociety Delphi consensus statement on new fatty liver disease nomenclature. Hepatology. 2023;78(6):1966-1986. PMID 37363821
  2. Younossi ZM, Golabi P, Paik JM, et al. The global epidemiology of nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH): a systematic review. Hepatology. 2023;77(4):1335-1347. PMID 36626630
  3. Riazi K, Azhari H, Charette JH, et al. The prevalence and incidence of NAFLD worldwide: a systematic review and meta-analysis. Lancet Gastroenterol Hepatol. 2022;7(9):851-861. PMID 35798021
  4. Le MH, Yeo YH, Li X, et al. 2019 Global NAFLD Prevalence: A Systematic Review and Meta-analysis. Clin Gastroenterol Hepatol. 2022;20(12):2809-2817.e28. PMID 34890795
  5. Amini-Salehi E, Letafatkar N, Norouzi N, et al. Global Prevalence of Nonalcoholic Fatty Liver Disease. Arch Med Res. 2024;55(6):103043. PMID 39094335
  6. Le P, Tatar M, Dasarathy S, et al. Estimated Burden of MASLD in US Adults, 2020 to 2050. JAMA Netw Open. 2025;8(1):e2454707. PMID 39821400
  7. Younossi ZM, Golabi P, Price JK, et al. The Global Epidemiology of NAFLD and NASH Among Patients With Type 2 Diabetes. Clin Gastroenterol Hepatol. 2024;22(10):1999-2010.e8. PMID 38521116
  8. Quek J, Chan KE, Wong ZY, et al. Global prevalence of NAFLD and NASH in the overweight and obese population. Lancet Gastroenterol Hepatol. 2023;8(1):20-30. PMID 36400097
  9. Ye Q, Zou B, Yeo YH, et al. Global prevalence, incidence, and outcomes of non-obese or lean NAFLD. Lancet Gastroenterol Hepatol. 2020;5(8):739-752. PMID 32413340
  10. Zamani M, Alizadeh-Tabari S, Ajmera V, et al. Global Prevalence of Advanced Liver Fibrosis and Cirrhosis in the General Population. Clin Gastroenterol Hepatol. 2025;23(7):1123-1134. PMID 39209202
  11. Hagström H, Shang Y, Hegmar H, et al. Natural history and progression of MASLD. Lancet Gastroenterol Hepatol. 2024;9(10):944-956. PMID 39243773
  12. Singh S, Allen AM, Wang Z, et al. Fibrosis progression in nonalcoholic fatty liver vs nonalcoholic steatohepatitis: meta-analysis of paired-biopsy studies. Clin Gastroenterol Hepatol. 2015;13(4):643-54.e1-9. PMID 24768810
  13. Angulo P, Kleiner DE, Dam-Larsen S, et al. Liver Fibrosis, but No Other Histologic Features, Is Associated With Long-term Outcomes of Patients With NAFLD. Gastroenterology. 2015;149(2):389-97.e10. PMID 25935633
  14. Hagström H, Nasr P, Ekstedt M, et al. Fibrosis stage but not NASH predicts mortality and time to development of severe liver disease in biopsy-proven NAFLD. J Hepatol. 2017;67(6):1265-1273. PMID 28803953
  15. Dulai PS, Singh S, Patel J, et al. Increased risk of mortality by fibrosis stage in NAFLD: Systematic review and meta-analysis. Hepatology. 2017;65(5):1557-1565. PMID 28130788
  16. Akbari C, Dodd M, Stål P, et al. Long-term major adverse liver outcomes in 1,260 patients with non-cirrhotic NAFLD. JHEP Rep. 2024;6(2):100915. PMID 38293684
  17. Noureddin N, Huang DQ, Bettencourt R, et al. Natural history of clinical outcomes and hepatic decompensation in MASLD. Aliment Pharmacol Ther. 2024;59(12):1521-1526. PMID 38571305
  18. Duell PB, Welty FK, Miller M, et al. NAFLD and Cardiovascular Risk: A Scientific Statement From the American Heart Association. Arterioscler Thromb Vasc Biol. 2022;42(6):e168-e185. PMID 35418240
  19. Mantovani A, Csermely A, Petracca G, et al. NAFLD and risk of fatal and non-fatal cardiovascular events: an updated systematic review and meta-analysis. Lancet Gastroenterol Hepatol. 2021;6(11):903-913. PMID 34555346
  20. Mantovani A, Petracca G, Beatrice G, et al. NAFLD and increased risk of incident extrahepatic cancers: a meta-analysis. Gut. 2022;71(4):778-788. PMID 33685968
  21. Mantovani A, Petracca G, Beatrice G, et al. NAFLD and risk of incident chronic kidney disease: an updated meta-analysis. Gut. 2022;71(1):156-162. PMID 33303564
  22. Simon TG, Roelstraete B, Khalili H, et al. Mortality in biopsy-confirmed NAFLD: results from a nationwide cohort. Gut. 2021;70(7):1375-1382. PMID 33037056
  23. Keam SJ. Resmetirom: First Approval. Drugs. 2024;84(6):729-735. PMID 38771485
  24. Harrison SA, Bedossa P, Guy CD, et al. A Phase 3, Randomized, Controlled Trial of Resmetirom in NASH with Liver Fibrosis. N Engl J Med. 2024;390(6):497-509. PMID 38324483
  25. Sanyal AJ, Newsome PN, Kliers I, et al. Phase 3 Trial of Semaglutide in MASH. N Engl J Med. 2025;392(21):2089-2099. PMID 40305708
  26. Bansal MB, Patton H, Morgan TR, et al. Semaglutide therapy for MASH: November 2025 updates to AASLD Practice Guidance. Hepatology. 2026;83(5):1326-1340. PMID 41201884
  27. Vilar-Gomez E, Martinez-Perez Y, Calzadilla-Bertot L, et al. Weight Loss Through Lifestyle Modification Significantly Reduces Features of NASH. Gastroenterology. 2015;149(2):367-78.e5. PMID 25865049
  28. Lassailly G, Caiazzo R, Ntandja-Wandji LC, et al. Bariatric Surgery Provides Long-term Resolution of NASH and Regression of Fibrosis. Gastroenterology. 2020;159(4):1290-1301.e5. PMID 32553765
  29. Aminian A, Al-Kurd A, Wilson R, et al. Association of Bariatric Surgery With Major Adverse Liver and Cardiovascular Outcomes in Patients With Biopsy-Proven NASH. JAMA. 2021;326(20):2031-2042. PMID 34762106
  30. Mózes FE, Lee JA, Vali Y, et al. Performance of non-invasive tests and histology for the prediction of clinical outcomes in patients with NAFLD. Lancet Gastroenterol Hepatol. 2023;8(8):704-713. PMID 37290471
  31. Aceituno L, Bañares J, Pons M, et al. The ANTICIPATE-NASH Models Stratify Better the Risk of Clinical Events Than Histology in MASLD Patients With Advanced Chronic Liver Disease. Gastroenterology. 2026;170(2):385-394. PMID 41212130
  32. Kleiner DE, Brunt EM, Van Natta M, et al. Design and validation of a histological scoring system for NAFLD. Hepatology. 2005;41(6):1313-21. PMID 15915461
  33. Donnelly KL, Smith CI, Schwarzenberg SJ, et al. Sources of fatty acids stored in liver and secreted via lipoproteins in patients with NAFLD. J Clin Invest. 2005;115(5):1343-51. PMID 15864352
  34. Marra F, Svegliati-Baroni G. Lipotoxicity and the gut-liver axis in NASH pathogenesis. J Hepatol. 2018;68(2):280-295. PMID 29154964
  35. Koliaki C, Szendroedi J, Kaul K, et al. Adaptation of hepatic mitochondrial function in humans with non-alcoholic fatty liver is lost in steatohepatitis. Cell Metab. 2015;21(5):739-46. PMID 25955209
  36. Schwabe RF, Tabas I, Pajvani UB. Mechanisms of Fibrosis Development in NASH. Gastroenterology. 2020;158(7):1913-1928. PMID 32044315
  37. Buzzetti E, Pinzani M, Tsochatzis EA. The multiple-hit pathogenesis of NAFLD. Metabolism. 2016;65(8):1038-48. PMID 26823198
  38. Loomba R, Schork N, Chen CH, et al. Heritability of Hepatic Fibrosis and Steatosis Based on a Prospective Twin Study. Gastroenterology. 2015;149(7):1784-93. PMID 26299412
  39. Romeo S, Kozlitina J, Xing C, et al. Genetic variation in PNPLA3 confers susceptibility to NAFLD. Nat Genet. 2008;40(12):1461-5. PMID 18820647
  40. Abul-Husn NS, Cheng X, Li AH, et al. A Protein-Truncating HSD17B13 Variant and Protection from Chronic Liver Disease. N Engl J Med. 2018;378(12):1096-1106. PMID 29562163
  41. Taylor RS, Taylor RJ, Bayliss S, et al. Association Between Fibrosis Stage and Outcomes of Patients With NAFLD: A Systematic Review and Meta-Analysis. Gastroenterology. 2020;158(6):1611-1625.e12. PMID 32027911
  42. Tilg H, Petta S, Stefan N, et al. Metabolic Dysfunction-Associated Steatotic Liver Disease in Adults: A Review. JAMA. 2026;335(2):163-174. PMID 41212550
  43. Torp N, Bech KT, Schnefeld HL, et al. Phosphatidylethanol and self-reported alcohol intake to subclassify individuals at risk of steatotic liver disease: an analysis of data from a prospective cohort study. Lancet Gastroenterol Hepatol. 2025;10(11):975-985. PMID 40945520
  44. Raverdy V, Tavaglione F, Chatelain E, et al. Data-driven cluster analysis identifies distinct types of metabolic dysfunction-associated steatotic liver disease. Nat Med. 2024;30(12):3624-3633. PMID 39653777
  45. Kwak M, Kim HS, Jiang ZG, et al. MASLD/MetALD and mortality in individuals with any cardio-metabolic risk factor: A population-based study with 26.7 years of follow-up. Hepatology. 2025;81(1):228-237. PMID 38739848