Once AMH expression is triggered independently of gonadotropins in fetal and postnatal life, FSH further increases testicular AMH output by inducing Sertoli cell proliferation and up-regulating AMH transcription (Fig. 2), which explains why patients with congenital central (hypogonadotropic) hypogonadism have low AMH serum levels that increase after treatment with exogenous FSH [42, 43]. Here, BRD2 is linked to hypogonadotropic hypogonadism.