Indeed, islets from diabetic Zucker rats have impaired GSIS due to defective glucose sensing associated with a reduction in the expressions of GLUT2 and GCK.7 Moreover, β‐cell–specific knockout of GLUT2 or GCK led to severe hyperglycaemia and infant death due to impaired GSIS and, conversely, re‐expression of GLUT2 in β cells rescued GLUT2‐null mice from infant death and restored normal GSIS.8, 9. Here, SLC2A2 is linked to Hyperglycemia.