Thus, insulin resistance, with the accompanying hyperinsulinemia, hyperglycemia, and other features of metabolic syndrome, acts as a mitogen by binding IRs on cancer cells, moreover, it also leads to increased IGF-1 synthesis in the liver and suppresses IGF binding proteins, which increases the bioavailability of this growth factor [40,44,45]. The gene discussed is IGF1; the disease is hyperinsulinism.