In the work at hand, we demonstrated that targeting CAV1 reduces cell adhesion to BMSCs, increases immunostimulatory surface markers and cytokines, disturbs redox homeostasis, inhibits autophagy flux, and reprograms glutamine metabolism in MM cells, thereby enhancing NK cell‐mediated cytotoxicity and bortezomib sensitivity (Figure 8H), and thus serving as a promising novel therapeutic approach for MM treatment. The gene discussed is CAV1; the disease is Miyoshi myopathy.