The increased understanding of the pathophysiology of MM revealed in 2015 the first two immunotherapeutic agents—the monoclonal antibodies (mAbs) targeting CD38 antigen and signaling lymphocytic activation molecule family member 7 (SLAMF7) on the surface of MM cells—and enlarged standard therapeutic regimens in relapsed or refractory MM (RRMM) [2,3,4]. Here, SLAMF7 is linked to Miyoshi myopathy.