Although the molecular pathogenesis of HCC can involve the inactivation of the TP53 gene [88,89], the absence of a TP53 somatic mutation in the majority of HCC cases [90] suggests that the inactivation can be achieved by other mechanism(s), such as p14ARF inactivation [91] or the amplification/overexpression of its specific inhibitors, MDM2 and MDM4 [92]. This evidence concerns the gene TP53 and hepatocellular carcinoma.