Finally, tyrosine kinase inhibitors mainly nilotinib produced potential therapeutic effects on the reactivation of the p53 gene in patients with CML as supported by Peterson et al.’s study that illustrated activation of the p53 gene in vitro and in vivo by a specific agent that prevented the binding of the p53 gene with negative regulators regarded as potential pathways for the cure of CML [31]. The gene discussed is TP53; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.