Bcr-Abl contributed to the phosphorylation of 4E-BP1 (inactivation) and induced the formation of eIF4F translation initiation complex, enhancing the cap-dependent protein expression, in which 4EBP1/eIF4E signaling pathway plays an important role in the pathogenesis of Ph+ leukemia [23]; accordingly, it may be a promising therapeutic target in Ph+ ALL. The gene discussed is EIF4EBP1; the disease is leukemia.