As a key tumor-suppressive transcriptional factor, although the inactivation of P53 alone is not sufficient to drive hepatocellular carcinoma (HCC) tumorigenesis, evidences has been provided that inactivation of P53 along with overexpression of oncogenes such as c-Myc makes hepatocytes more prone to oncogenic transformation and to acquire CSCs characteristics so to increase stem genes expression (Liu et al., 2017). The gene discussed is TP53; the disease is neoplasm.