Over the last two decades, the incorporation of proteasome inhibitors, immunomodulatory agents, CD38-targeted antibodies, and BCMA-directed therapies into frontline and relapse regimens has markedly improved survival outcomes in MM, particularly when used in multidrug combinations, as summarized in Figure 3. Given the rapidly evolving therapeutic landscape of MM, driven by shifting biological targets and increasingly potent pharmacologic strategies, there is a growing need to refine and update prognostic markers so that they better capture treatment-related biological dynamics. The gene discussed is CD38; the disease is Miyoshi myopathy.