By promoting the ubiquitination and degradation of the native or mutant BCR-ABL, SH2-U-box blocked BCR-ABL-dependent signaling pathway, and thus inhibited cell proliferation and induced cell apoptosis in both imatinib-sensitive and resistant CML cells (Fig. 7). Here, ABL1 is linked to chronic myelogenous leukemia, BCR-ABL1 positive.