These factors may induce DNA damage, epigenetic alterations and cancer-related mutations, leading to the silencing of tumor suppressors (e.g. TP53, CDH1, RASSF1) and the activation of oncogenes (e.g. MYC, VEGFA, MAPK7), which eventually contribute to HCC progression [3–6]. The gene discussed is TP53; the disease is neoplasm.