The proposal that LH and FSH deficiencies associated with hPRL are mediated by a direct inhibitory effect of PRL on GnRH neurons was supported by the demonstration that recombinant PRL administration suppressed pulsatile endogenous LH secretion in healthy women [6] and that pulsatile GnRH replacement can reverse hypogonadotropic hypogonadism and restore fertility in women and men with hPRL [7–9]. This evidence concerns the gene GNRH1 and hypogonadotropic hypogonadism.