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. The gene discussed is HDAC9; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.