To investigate the role of potential signaling pathways in sustaining Ph+ B-ALL cells upon the treatment of ABL TKI, we treated a widely used human Ph+ B-ALL cell line SUP-B15 with dasatinib for 6 h and confirmed that the phosphorylation of the BCR-ABL, as well as its classic downstream STAT5 [26] and AKT, was inhibited (Fig. 1a). The gene discussed is ABL1; the disease is acute lymphoblastic leukemia.