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. This evidence concerns the gene ABL1 and chronic myelogenous leukemia, BCR-ABL1 positive.