Skeletal muscle (approximately 80 percent of postprandial glucose disposal) develops GLUT4 translocation defects that limit uptake (47–49); the liver maintains gluconeogenesis/glycogenolysis despite hyperinsulinemia, sustaining hyperglycemia; and adipose tissue insulin resistance augments lipolysis and circulating FFAs, further propagating insulin resistance across organs (50). The gene discussed is INS; the disease is hyperinsulinism.