The PI bortezomib has been reported to provoke programmed cell death in MM cells by producing an increase of proapoptotic BIM and a decrease of the pro-survival protein, MCL-1 [79,80], while MM cells quickly experience apoptosis upon genetic deletion of MCL-1 or BCL-2 [81] or use of BCL-2 or MCL-1 inhibitors [82,83,84]. This evidence concerns the gene PROS1 and Miyoshi myopathy.