In support of the former possibility, studies in animals have shown that intrauterine hyperandrogenemia induces morphological changes in kisspeptin/neurokinin B/dynorphin neurons and increases kisspeptin-positive cells in the hypothalamus [24,25]; furthermore, the exogenous AMH administration during gestation alters the hypothalamic GnRH network [47] (in which NKB and KISS1 are major components). The gene discussed is PDYN; the disease is polycystic ovary syndrome.