When we treated the drug-resistant BaF3-p210T315I cells, similar to non-resistant K562 cells, TGI1002 disrupted the association of SET with PP2A, down-regulated phosphorylated PP2Ac, increased PP2A activity and antagonized the inhibitory effects of OA on PP2A (Figure 4C and 4D), suggesting that TGI1002 may be active and useful for the treatment of drug-resistant CML with T315I mutation of BCR-ABL. Here, SET is linked to chronic myelogenous leukemia, BCR-ABL1 positive.