Consistent with these notions, we demonstrated that blockade of MEK1/2 functions reactivates the anti-oncogenic function of normal BCR kinase as well as converts normal ABL1 kinase from a cytoplasmic oncogenic to a nuclear tumor-suppressive effector thus enhancing the antitumor effects of ATO via activation of BCR-MYC and ABL1-p73 signaling pathways (Fig. 7D). This evidence concerns the gene MYC and neoplasm.