Zhou et al. explored the effect of the PI3K-specific inhibitor ZSTK474 on K562/A02 cells and their results showed that ZSTK474 reversed the resistance of K562/A02 cells to ADM and imatinib by downregulating P-gp expression; accordingly, the target of ZSTK474 for CML treatment is PI3K [26]. This evidence concerns the gene PGP and chronic myelogenous leukemia, BCR-ABL1 positive.