As a consequence, IRS-1 phosphorylation is inhibited leading to lower binding of phosphatidylinositol 3-kinase to IRS-1 and lower translocation of glucose transporter (GLUT-4) to the membrane, stimulated by insulin, with subsequent worsening of hyperglycemia and hyperinsulinemia [4,13,37]. The gene discussed is INS; the disease is hyperinsulinism.