The combined inhibition of HDACs and the proteasome leads to a significant decrease in both efficacy and metabolism of CML-derived BCR/ABL-expressing K562 cells than either drug alone, indicating that treatment with concomitant use of HDAC and proteasome inhibitors could be a successful approach in CML therapy. This evidence concerns the gene BCR and chronic myelogenous leukemia, BCR-ABL1 positive.