Our data indicate that KLF5-expression increased apoptosis of leukemic B-cell precursors, particularly in imatinib-resistant Ph+ B-ALL cells without affecting the differentiation of either leukemic or normal B-cell lymphopoiesis, suggesting that KLF5 may be a possible target in overcoming the resistance to ABL TKI seen in a fraction of Ph+ B-ALL patients. This evidence concerns the gene ABL1 and acute lymphoblastic leukemia.