A previous study showed that inactivating mutations of the genes encoding NKB or its receptor (NK3R) in humans led to a state of central hypogonadism similar to that of the inactivating mutations of the kisspeptin pathway [47], indicating that the NKB signal is indispensable for kisspeptin secretion in KNDy neurons. The gene discussed is TAC3; the disease is hypogonadotropic hypogonadism.