However, in the present study, we demonstrate for the first time that the sole overactivation of GnRH neurons for a short lag of time in young adult mice is sufficient to entrain long-term deregulation of GnRH neuronal physiology cascading in a long-lasting state of neuroendocrine dysfunction, hyperandrogenism, and excessive AMH secretion. The gene discussed is AMH; the disease is hyperandrogenism.