This results in increased GABAergic PSC amplitude and frequency, increased firing, persistently elevated GnRH/LH release frequency, and reduced progesterone (P) negative feedback prior to androgen (T) excess and reproductive impairments (including disrupted reproductive cycles) that mimic those of polycystic ovary syndrome (PCOS), the most common endocrinopathy in women of reproductive age and the leading cause of female infertility (35, 59, 77–80). This evidence concerns the gene PLOD1 and polycystic ovary syndrome.