The addition of proteasome inhibitors to DACi treatment regimens enhances the sensitivity of MM cells to DACi to induce mitochondrial dysfunction, caspase-9, caspase-8, and caspase-3 activation, and poly (ADP-ribose) polymerase degradation, which is associated with NF-κB inactivation, c-Jun NH2-terminal kinase activation, p53 induction, caspase dependent cleavage of p21CIP1, p27KIP1, and Bcl-2, and cyclin D1 downregulation [216]. This evidence concerns the gene CDKN1B and Miyoshi myopathy.