Excessive insulin secretion triggered by IR can promote androgen secretion via three pathways, which ultimately results in hyperandrogenemia: direct activation of 17-β hydroxylase in follicular membrane cells, which promotes androgen production; stimulation of luteinizing hormone production via insulin receptors in the pituitary gland, which further enhances androgen production in the ovaries; inhibition of the synthesis of hepatic sex hormone-binding globulins, which leads to an increase in free androgen levels in the bloodstream [62, 63]. This evidence concerns the gene INS and polycystic ovary syndrome.