The fundamental role of MAT1A downregulation in the pathogenesis of liver injury and HCC was further proved by the demonstration that, in MAT1A-KO mice, chronic SAM deficiency not compensated by MAT2A induction provokes precocious hepatomegaly with macrovesicular steatosis, involving up to 75% of hepatocytes, followed by mononuclear cell infiltration in periportal areas and HCC at eight months of age [59]. This evidence concerns the gene MAT1A and hepatocellular carcinoma.