This process may be driven by therapeutic selection pressures (e.g., loss of CD38 after daratumumab exposure56) or may already exist at baseline in high-risk patients (e.g., high circulating tumor cells with genomic complexity).36 Because most current MM therapies target plasma cell biology, these transformed subclones become increasingly resistant and less sensitive to such approaches (Figure 7). The gene discussed is CD38; the disease is Miyoshi myopathy.