Mouse models with genetic ablation of the methionine adenosyltransferase 1A gene (Mat1a), which encodes the enzyme that catalyzes the conversion of methionine to SAM, showed lower hepatic SAM level, higher lipogenesis and oxidative stress, and consequently were predisposed to the NAFLD-related HCC development [65,66]. This evidence concerns the gene MAT1A and hepatocellular carcinoma.