The carcinogenic effect of chronic hyperinsulinemia is attributed to (i) stimulation of MAPK and PI3K/Akt pathways; (ii) an increase in the bioavailability and synthesis of insulin-like growth factor 1 (IGF-1); and (iii) overexpression of vascular endothelial growth factor (VEGF), favoring pro-angiogenic pathways [28,31,34,35,36]. Here, IGF1 is linked to hyperinsulinism.