Mechanisms of bort resistance in MM have been implicated in both intrinsic changes, including MM cells and their subclone heterogeneity, and the protective efficacy of BMSCs.6, 7, 30 We demonstrated that primary CD138+ plasma cells from patients with MM underwent spontaneous apoptosis in vitro, suggesting that plasma cells in vivo reacquired susceptibility when separated from the BM microenvironment in vitro. The gene discussed is SDC1; the disease is Miyoshi myopathy.