Interestingly, HDAC inhibitor VPA treatment in the K562 cell line model also resulted in the inhibition of Notch signalling/Hes-1 and overexpression of BCR-ABL activity, further confirming the antagonistic interaction between the Notch signalling pathway and BCR-ABL in the blastic phase of CML, which was seen with GSI treatment of K562 cells. This evidence concerns the gene BCR and chronic myelogenous leukemia, BCR-ABL1 positive.