Sclerostin, encoded by the SOST gene, antagonizes Wnt signaling in both osteocytes and osteoblasts by binding to the LRP5/6 coreceptor and preventing bone formation.[9,10] High-bone-mass syndromes are thought to be caused by inactivating mutations of SOST (sclerosteosis and van Buchem’s disease).[11] Animal studies have indicated that sclerostin inhibition increases bone mass by stimulating bone formation and inhibiting bone resorption.[12]. This evidence concerns the gene SOST and hyperostosis corticalis generalisata.