SOST and osteoporosis: In mice, glucocorticoids increased the expression of Sost, the gene encoding sclerostin production.11 In female KO mice lacking Sost and thus characterized by activation of Wnt/β‐catenin signaling, bone mass and strength were maintained in conditions of glucocorticoid excess.11 Moreover, antibodies against sclerostin in mice prevented glucocorticoid‐induced osteoporosis and appeared to maintain osteoblast activity.12