During fasting, this delicate insulin-glucagon balance becomes increasingly dependent on hepatic responsiveness and insulin sensitivity. As a result of T1D, however, this defense mechanism is impaired at an early stage [8-10], and the combination of relative insulin deficiency and variable insulin resistance, particularly in those using exogenous insulin, disrupts normal hepatic glucose release and increases susceptibility to hypoglycemia. The gene discussed is INS; the disease is type 1 diabetes mellitus.