Finally, PMIBcr/Abl‐R6 competitively releases p53, which is usually wild type and inactive in leukemias, playing the role of an “MDM2 switch” that changes from suppression of the cancer suppressor p53 to suppression of the oncoprotein Bcr/Abl, efficiently promoting apoptosis via multiple mechanisms. This evidence concerns the gene BCR and leukemia.