Similar alterations have been described in MATO-KO mice, a NASH-HCC animal model that in the absence of Mat1a cannot synthesize SAM and presents steatosis involving 25–50% of hepatocytes and mononuclear cell infiltration in periportal areas, at eight months, and HCC at 18 months of age [23,138,139,140]. This evidence concerns the gene MAT1A and metabolic dysfunction-associated steatohepatitis.