Though Imatinib and other TKIs are potent inhibitors for CML, Ph+ B-ALL patients or established cell lines from these patients were resistant to these conventional TKIs, most likely due to high and constant expressions of phosphorylated BCR-ABL and its substrate proteins, STAT5 and CrkL, or partly due to Imatinib-induced T351I mutation in ABL domain [8. The gene discussed is BCR; the disease is acute lymphoblastic leukemia.