While augmented hepatic gluconeogenesiss [36], impaired beta-cell response to glucose, and peripheral insulin resistance [37] all predispose CKD patients to hyperglycemia, counteractive mechanisms such as deficient renal gluconeogenesis, impaired renal insulin clearance and degradation, anorexia and diminished glycogen stores, and deficiency in immediate counter-regulatory catecholamine response can render patients as hypoglycemic [7]. The gene discussed is INS; the disease is chronic kidney disease.