In this review, we synthesize and discuss the available literature to provide an updated understanding of the complex role that CHIP plays in altering the MM microenvironment, and the resulting impact on standard MM treatments, autologous stem cell transplant (ASCT) and B-cell maturation antigen (BCMA)-targeted therapy/CAR-T, and the important role of immunomodulatory drug (IMiD) maintenance therapy in clinical outcomes. The gene discussed is TNFRSF17; the disease is Miyoshi myopathy.