Coutinho and Kauffman concluded that a hyperactive GnRH neural circuit, including an increase in GnRH neuron activity, an increase in stimulatory gamma amino butyric acid (γ-aminobutyric acid, GABA)-ergic (GABAergic) innervation, and postsynaptic currents onto GnRH neurons, as well as an increased secretion of kisspeptin, favor a neuroendocrine basis for either the etiology or phenotype of PCOS [78]. The gene discussed is GNRH1; the disease is polycystic ovary syndrome.