For example, ADH1A triggered oncogenic transformation of hepatocytes leading to poor survival,[21] whereas extracellular PEDF inhibited angiogenesis in HCC by inducing lipid metabolic disorders.[22] These insights into the molecular mechanisms and genes markers involved in the pathogenesis of HCC have extended our understanding of the metabolic profile of HCC. This evidence concerns the gene ADH1A and hepatocellular carcinoma.