On the other hand, insulin has been shown to repress insulin-like growth factor-1 binding protein (IGFBP-1) synthesis in a direct, rapid, and complete way in both the liver and the ovaries, allowing for greater IGF-1 availability, which in turn boosts insulin activity not only in the liver—further contributing to lower SHBG levels—but also in the ovaries, reinforcing PCOS pathophysiology [77]. This evidence concerns the gene INS and polycystic ovary syndrome.