Impairment of the p14CDKN2A-MDM2-p53 cascade, whose final effectors are the Bax/Bcl-2 proteins, has been implicated in defective apoptotic responses to genotoxic damage and, thus, to anticancer agents (in most cases, melanoma cells present concurrent high expression levels of Bax/Bcl-2 proteins, which may contribute to further increasing their aggressiveness and refractoriness to therapy) [14,15]. The gene discussed is BAX; the disease is melanoma.