At any rate, IR-hyperinsulinemia activity leads to hyperandrogenemia, which in turn induces pro-IR structural and functional modifications in key insulin target tissues, including decreased amount of more oxidative, insulin-sensitive type I muscle fibers, and increased amount of more glycolytic, less sensitive type II fibers [40], as well as elevated lipolysis in adipocytes, favoring free fatty acid- (FFA-) mediated IR [45], perpetuating the IR-hyperinsulinemia-hyperandrogenemia feedback [7]. This evidence concerns the gene INS and polycystic ovary syndrome.