On the other hand, even though neuroendocrine regulation in PCOS shows robust differences, ranging from GnRH pulsatility to hormonal feedback and neuropeptide signaling, further modulatory effects conferred by metabolic dysregulation (e.g., insulin and leptin resistance and hyperandrogenism) indirectly define potential physiopathologically relevant causes [92]. The gene discussed is LEP; the disease is polycystic ovary syndrome.