It was suggested that hyperinsulinemia contributes to cancer development through direct effects of insulin on growth-promoting signaling, and indirectly through the effects of prolonged hyperinsulinemia that increase the availability of bioactive IGF-1 via the reduction of circulating levels of the proteins (IGF binding proteins) that normally bind IGF-1 and make it biologically unavailable. The gene discussed is INS; the disease is Hyperinsulinemia.