For example, in A/J mice, a strain that exhibited a more methylated phenotype in the normal livers and a mild NAFLD-like liver injury, the CFD diet caused hypomethylative changes in CpG islands, whereas in WSB/EiJ mice, which are characterized by a less methylated original hepatic phenotype and severe NASH-like liver injury, feeding the CFD diet caused profound hypermethylative changes driven by up-regulation of DNMT1 and DNMT3A and concurrent inhibition of gene expression. Here, DNMT3A is linked to metabolic dysfunction-associated steatohepatitis.