Indeed, Ohtsubo and colleagues [63] found that deficiency in N-acetylglucosaminyltransferase or posttranslational modification with glycan-ligand mimetics strongly lower the Glut-2 cell-surface half-life and subsequently lead to premature endocytosis with redistribution into endosomes and lysosomes for rapid degradation, which has been attributed to prolonged hyperglycaemia. The gene discussed is SLC2A2; the disease is Hyperglycemia.