The pathogenesis of HCC disease was hypothesized to start with the dysfunctionality of cirrhotic or non-cirrhotic hepatocytes caused by the mutations induced by the HBV conjugated to further risk factors, such as aflatoxin B1, and involves an accumulation of genetic variations, including inactivation of tumor suppressor genes, such as TP53, and the activation of proliferation pathways, such as Wnt/FZD/β-catenin and PI3K/Akt/mTOR [5,7,8,9]. This evidence concerns the gene TP53 and hepatocellular carcinoma.