In addition, hyperinsulinemia mediates the production of IGF-1 (Figure 2B), inhibits the production of IGFBP in the liver, increases the bioavailability of IGF-1 and stimulates further tumor growth through excessive activation of the PI3K-Akt-mTOR pathway and Ras-MAPK pathway (114). The gene discussed is IGF1; the disease is neoplasm.