When the proteomes of human NASH and HCV-associated HCCs were compared, altered proteins and enzymes involved in lipid, cholesterol, and bile acid biosynthesis, fatty acid oxidation and catabolism, mitochondrial dysfunction, and the downstream molecules of activated SREBP-LXRα, NRIP1, and inhibited PPARs was specific to NASH, but not the virus-associated HCC [14]. This evidence concerns the gene NR1H3 and metabolic dysfunction-associated steatohepatitis.