Given that the survival and proliferation of CML cells were “addicted” to the constitutively active BCR-ABL37, 38, we asked whether SH2-U-box-caused downregulation of BCR-ABL or T315I mutant can inhibit K562 or K562R or affect cells’ response to imatinib, the first line therapy of CML. The gene discussed is ABL1; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.