The lack of FSH stimulation during fetal and neonatal life is responsible for the decreased Sertoli cell numbers and low AMH expression in patients with congenital hypogonadotropic hypogonadism.[44, 45] The increase in serum AMH in those patients receiving FSH may be useful to monitor treatment efficacy [42, 43, 49]. The gene discussed is AMH; the disease is congenital hypogonadotropic hypogonadism.