GC is known to affect the bone by uncoupling bone resorption and bone formation, resulting in increased bone resorption by inhibiting gonadal steroids, increased urinary calcium excretion by inhibiting intestinal and renal calcium reabsorption, and secondary hyperparathyroidism and reduced bone formation by inhibiting type I collagen, osteocalcin, insulin-like growth factors, and bone matrix proteins, receptor activator for nuclear factor kappa B ligand (RANK-L (18, 19). The gene discussed is TNFSF11; the disease is secondary hyperparathyroidism.