In clinical practice or clinical trials, proteasome inhibitors, immunomodulatory drugs, and monoclonal antibodies (MoAbs) against CD38 or SLAMF7 have been combined to achieve significant remission rates in newly diagnosed and relapsed multiple myeloma (MM) patients.[1] Unfortunately, however, in most MM patients, relapse is unavoidable due to cell‐intrinsic heterogeneity, clonal evolution, and/or acquired resistance.[2] Therefore, novel biological targeted therapies are still urgently needed to improve MM treatment. The gene discussed is CD38; the disease is Miyoshi myopathy.