The insulin signaling defect is due to serine phosphorylation of insulin receptors and IRS-1 secondary to intracellular serine kinases in PCOS, which results in decreased insulin-mediated activation of PI3-K and resistance to the metabolic actions of insulin has been postulated that the same kinase may inhibit insulin signaling in PCOS [29]. This evidence concerns the gene IRS1 and polycystic ovary syndrome.