Prospective, multicenter studies involving larger, ethnically diverse MM cohorts are warranted to externally validate the prognostic model, and functional studies employing in vivo MM models (e.g., patient‐derived xenografts) should confirm the causal role of CREB3L2 and its downstream effectors in regulating angiogenesis, proliferation, and apoptosis. The gene discussed is CREB3L2; the disease is Miyoshi myopathy.