GLUT3 has a much higher affinity for glucose than GLUT1 (by a factor of 7), and the cerebral extracellular glucose concentration (approximately 2 mM) is systematically higher than the Km of GLUT3 (<1 mM), suggesting that GLUT3 expression is not a limiting step during variations in cerebral glucose consumption (during neuronal activation or hypoglycemia, for example) [58,59]. Here, SLC2A1 is linked to Hypoglycemia.