Indeed, the mechanisms of p53 modulation in CML pathogenesis appeared to be highly complex and, as a consequence, the development of strategies to reactivate p53 in CML and the effects of drugs that modulate IκB-α degradation (proteasome inhibitors) on p53 require further experimental investigations but may represent a new challenging approach to cure Ph+ leukemias. The gene discussed is NFKBIA; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.