We therefore hypothesized that NK3R antagonism would affect LH secretion in women with PCOS through modification of aspects of its pulsatile secretion, and that a functionally upstream site of action would not prevent the stimulatory effect of kisspeptin on LH secretion, but that the LH response to kisspeptin would be modified, indicating a role of NK3R signalling in the regulation of that response to circulating oestradiol levels. The gene discussed is PLOD1; the disease is polycystic ovary syndrome.