A variety of mechanisms have been proposed to explain the role of MetS in cancers including regulation of the insulin-like growth factor-1 (IGF-1) pathway, existence of hyperinsulinemia and insulin resistance, process of adipokine production, angiogenesis promotion, glucose malutilization, and oxidative stress/DNA damage, which can synergistically increase the cancer risk rather than just individual components (29, 30). This evidence concerns the gene IGF1 and hyperinsulinism.