This may also explain why much less glucose is required to maintain euglycemia in infants with AKT2 p.Glu17Lys, in which the metabolic defect may be failure to derepress gluconeogenesis during fasting, than in those with hyperinsulinism, in whom there is also inappropriate disposal of glucose into skeletal muscle and adipose tissue mediated by GLUT4. Here, SLC2A4 is linked to hyperinsulinism.