In children with endogenous Cushing’s, excess cortisol profoundly disrupts bone metabolism through the same mechanisms as exogenous glucocorticoids, but resolution of hypercortisolemia—most often via transsphenoidal surgery for pituitary adenomas—allows gradual normalization of bone turnover, GH/IGF-I, sex steroid, calcium, and PTH homeostasis [31]. The gene discussed is PTH; the disease is pituitary gland adenoma.