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While metabolic triggers such as obesity and insulin resistance are key drivers of MASLD, growing evidence has identified defects in intracellular quality control\u2014namely impaired autophagy\u2014as central mechanisms governing disease progression. Autophagy, including selective lipophagy and mitophagy, plays a crucial role in hepatic lipid turnover and mitochondrial homeostasis. In MASLD, disruption of these processes contributes to lipid accumulation and oxidative stress, leading to hepatocellular damage (ballooning), fibrogenesis, and HCC. Experimental studies linked impaired autophagic flux to liver injury, and emerging evidence from human genetics suggests that inter\u2010individual inherited variation influences MASLD susceptibility by impairing autophagy. Specifically, main genetic MASLD modifiers such as the p.I148M variant of Patatin\u2010like phospholipase domain\u2010containing protein 3 (\n                    <jats:italic>PNPLA3<\/jats:italic>\n                    ) and loss\u2010of\u2010function and hypomorphic variants in autophagy\u2010related gene 7 (\n                    <jats:italic>ATG7<\/jats:italic>\n                    ), a core autophagy gene, predispose to ballooning, fibrosis, and HCC. By outlining emerging therapies that restore autophagic flux and reduce steatosis, lipotoxicity, and fibrosis, we propose an integrated precision\u2010medicine model based on genetics and autophagy dynamics biomarkers, offering a new framework for personalized therapeutics.\n                  <\/jats:p>","DOI":"10.1111\/liv.70816","type":"journal-article","created":{"date-parts":[[2026,7,29]],"date-time":"2026-07-29T09:16:56Z","timestamp":1785316616000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Autophagy in\n                    <scp>MASLD<\/scp>\n                    : A Metabolic and Precision Medicine Perspective"],"prefix":"10.1111","volume":"46","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-7153-2256","authenticated-orcid":false,"given":"Alessandra","family":"Cazzaniga","sequence":"first","affiliation":[{"name":"Department of Pathophysiology and Transplantation Universit\u00e0 degli Studi di Milano  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