While the potential contribution of kisspeptin and NKB in PCOS is assumed to be mainly central acting, recent studies show that locally deregulated expression of KISS1 and NKB at the level of granulosa cells may also contribute to the disruption in gonadal to central feedback of the hypothalamic-pituitary-ovarian axis that is characteristic in PCOS [53]. This evidence concerns the gene TAC3 and polycystic ovary syndrome.