Chronic hyperinsulinemia suppresses hepatic synthesis of insulin-like growth factor binding proteins, thereby increasing free Insulin-like Growth Factor-1 (IGF-1) bioavailability, which subsequently activates IGF-1 receptors (IGF-1R) to promote cellular proliferation and metastatic potential (Djiogue et al., 2013). This evidence concerns the gene IGF1 and hyperinsulinism.