Although these progresses in immune therapies and their application for the treatment of MM have not succeeded until recently, these therapeutic strategies have finally attained a breakthrough with the development of the MoAb therapies targeting surface molecules, expressed in MM cells, such as elotuzumab, a humanized anti-CS1/SLAMF7 monoclonal antibody, and daratumumab, a humanized anti-CD38 monoclonal antibody, both of which have been approved in the treatment of relapsed or refractory MM (RRMM) patients who received at least three prior therapies including PIs and iMiDs [40–43]. The gene discussed is CD38; the disease is Miyoshi myopathy.