Murphy et al. [121] found that tissue repair genes, such as fibroblast growth factor receptor 2 (FGFR2) and caspase 1 (CASP1), were hypomethylated and overexpressed, whereas a gene in one-carbon metabolism, methionine adenosyl methyltransferase 1A (MAT1A), which generates SAM, was hypermethylated and underexpressed in liver biopsies from patients with advanced NAFLD. This evidence concerns the gene MAT1A and metabolic dysfunction-associated steatotic liver disease.