In high-fat diet-induced NAFLD mouse models, increased liver ACSL3 expression is concurrent with lipid vacuolization and inflammation (Mossmann et al., 2023). In vitro, silencing ACSL3 in hepatocytes reduces oleic acid-induced lipid accumulation and steatosis, implicating it in driving steatosis (Klasson et al., 2022). This evidence concerns the gene ACSL3 and metabolic dysfunction-associated steatotic liver disease.