In Ph+ leukemia cases, to counteract the notably mutation‐free Bcr/Abl‐independent resistance, activating p53 has been proven to be a promising therapeutic approach.[22] Rossana and colleagues proved that Bcr/Abl augments MDM2 expression through its downstream pathway, which results in wild‐type p53 inactivation and then dysfunction in Ph+ leukemias.[23] Additionally, Abraham et al.[24] showed that activating p53 in CML could eliminate cancer stem cells. The gene discussed is BCR; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.