In individuals with visceral obesity, there is a decrease in the insulin-mediated suppression of lipolysis, leading to increases in circulating FFAs concentrations that contribute to both peripheral and hepatic insulin resistance either by impairing insulin signalling pathways, by competitive inhibition of muscle glucose uptake, by stimulation of endogenous glucose production, thus contributing to hepatic insulin resistance, or by combination of mentioned mechanisms [6, 7, 9, 10]. The gene discussed is INS; the disease is Insulin resistance.