Accordingly, the introduction of proteasome inhibitors, which hamper protein clearance inside plasma cells already overwhelmed by the production of immunoglobulins [7,8]; of lenalidomide-based treatments, which target for degradation essential factors for MM cell survival, including the Ikaros family zinc finger proteins 1 and 3 (IKZF1 and IKZF3), but also interfere with angiogenesis [9,10]; and most recently, of anti-CD-38 monoclonal antibodies [11,12,13,14], which have led to an important improvement in the survival of MM patients. This evidence concerns the gene IKZF1 and Miyoshi myopathy.