Mechanistically, FGL1 was found to enhance ERK1/2 phosphorylation, leading to increased expression of mature sterol regulatory element-binding protein 1 (mSREBP-1) and lipid synthesis-related enzymes like fatty acid synthase (FAS) and acetyl-CoA carboxylase-1 (ACC-1), thereby promoting hepatic lipid accumulation and driving NAFLD progression [52]. The gene discussed is ACACA; the disease is metabolic dysfunction-associated steatotic liver disease.