Accordingly, bortezomib induces a “BRCAness” state in MM cells, since it gives raises to the accumulation of polyubiquitylated proteins in the cytoplasm, depletion of nuclear-free ubiquitin, and, as a consequence, the abrogation of H2AX polyubiquitylation, an essential step for the recruitment of BRCA1 and RAD51 to the sites of DNA DSBs and the initiation of HR-mediated DNA repair. This evidence concerns the gene RAD51 and Miyoshi myopathy.