BCR/ABL1 fusion protein disturbed downstream signaling pathways, causing enhanced proliferation, differentiation arrest, and resistance to cell death.[20,21] TKIs were the most successful class of molecular targeted therapy for CML, but there were rarely Ph+ AML patients benefit from TKI therapy.[3,6] Neuendorff et al[17] suggested that treatment with a single molecularly targeted (TKI) agent might not be sufficient for disease control of Ph+ AML, so they thought that TKI therapy could not be routinely recommended as a part of first-line therapy. This evidence concerns the gene BCR and acute myeloid leukemia.