Genetic inhibition of BCMA with dox-inducible shBCMA led to a significant decrease in established MM tumor size in both models (Fig. 1, D and E; and Fig. S1 C), further demonstrating that BCMA signaling can act as a master regulator of MM survival and is independent of heterogeneous genetic mutations. This evidence concerns the gene TNFRSF17 and Miyoshi myopathy.