In the drug screen, we found that arsenic trioxide (ATO) was able to down-regulate both RNF6 and VIM (Fig. 1O) and suppressed CML cell proliferation (Fig. S6A), and the overexpression of either RNF6 or VIM could rescue the cleavage and activation of PARP and caspase-3 induced by ATO (Fig. S6B, C), the hallmarks of apoptosis, suggesting ATO induces CML cell death partly via the RNF6/VIM axis. Here, CASP3 is linked to chronic myelogenous leukemia, BCR-ABL1 positive.