Such results are in agreement with prior reports regarding growth inhibition of HDACi plus TKIs on CML cells.12 Furthermore, it was suggested that CAY10683 combined with IM treatment had synergistic effects on the cells resistant to IM mainly through inhibiting HDAC2 and that the PI3K/Akt signal transduction pathway modulated HDAC2 regulation on CML cells resistant to IM. Here, AKT1 is linked to chronic myelogenous leukemia, BCR-ABL1 positive.