It is usually acknowledged that i-IGT, characterized by the elevation of postload glucose during OGTT and normal FPG, is largely related with defect of the first-phase insulin secretion and peripheral insulin resistance (IR), while i-IFG, characterized by moderately increased FPG and normal postload glucose, is mainly caused by increased hepatic glucose production resulting from hepatic IR [37]. The gene discussed is INS; the disease is Hepatitis.