Promising clinical data with anti-CD38 monoclonal antibodies daratumumab and isatuximab and the anti-signaling lymphocyte activation marker F7 (SLAMF7) antibody elotuzumab, CD3-engaging bispecific antibodies redirecting T-cells to MM targets such as CD38, the orphan G protein-coupled receptor GPRC5D, or the B-cell maturation antigen (BCMA)/CD269, as well as chimeric antigen receptor (CAR)-T cells or natural killer (NK) cells have contributed to a renewed hope regarding the potential of overcoming cancer drug resistance in MM [2]. The gene discussed is GPRC5D; the disease is Miyoshi myopathy.