Indeed, such studies have uncovered a link between genetically determined circulating sclerostin levels and bone mineral density as well as fracture risk,126 although the original identification of sclerostin as a regulator of bone mass arose from genetic disorders, namely Van Buchem’s disease and Sclerosteosis.127 Consistently, anti-sclerostin antibodies such as romosozumab have proven effective in treating osteoporosis in patients,128 further underlining the validity of this tool. The gene discussed is SOST; the disease is hyperostosis corticalis generalisata.