We also investigated the methylation status of individual genes, which play important roles in the pathogenesis of human NAFLD, at promoter CpG islands for lipogenic (HMG-CoA reductase, HMGCR; and fatty acid synthase, FASN), inflammatory (NFkB1and c-Jun), and apoptosis (Bcl-2 and Caspase 3) targets. Here, JUN is linked to metabolic dysfunction-associated steatotic liver disease.