This is an important obstacle to the use of doses that maximize its antineoplastic properties.39 Moreover, when the p53 tumor suppressor is mutated and inactive, which is the case in more than half of cancers, the effectiveness of such treatments is significantly compromised.41 This is why restoring tumor cell sensitivity to anti-cancer agents in p53-negative tumors and at the same time protecting normal tissues from chemotherapy-induced side effects, or at least decreasing toxicity towards them, is a very attractive strategy in oncology. The gene discussed is TP53; the disease is cancer.