Suppressed activity of osteoblasts occurs because of aberrant Wnt signaling in MM.(30) Inhibitors of the canonical Wnt pathway, such as sclerostin, Dickkopf‐like protein 1 (DKK‐1), and soluble frizzled‐related proteins (sFRP), inhibit bone formation.(31, 32) Sclerostin, a glycoprotein produced by osteocytes, impedes the activation of the canonical Wnt pathway, inhibiting osteoblast maturation and impairing bone mineralization.(33, 34, 35) Furthermore, it induces apoptosis of osteoblasts through caspase activation and increases the RANKL/OPG ratio, resulting in enhanced osteoclastogenesis. This evidence concerns the gene SOST and Miyoshi myopathy.