Drug resistance of MM has been shown to be mediated through several mechanisms including loss of CD38 expression, BCMA expression, proteasome subunit β type 5 (PSMB5) point mutation or overexpression, and Cereblon (CRNB) down regulation, all of which help to produce MM stem-like cells (MMSCs). The gene discussed is TNFRSF17; the disease is Miyoshi myopathy.