IR and hyperandrogenism (HA) along with insulin secretory defects, post-receptor defect in insulin signalling, low-grade inflammation, high carbohydrate consumption, hypothalamic–pituitary axis abnormalities and disrupted folliculogenesis contribute to the reproductive and metabolic dysfunctions in PCOS [5,10,16,17,18]. This evidence concerns the gene INS and polycystic ovary syndrome.