In addition to the potential role of altered N-glycosylation of the EAAT1 and EAAT2 glutamate transporters and the GluA2 subunit in glutamatergic signaling abnormalities in schizophrenia, abnormal N-glycosylation of kainate receptor subunit GluK2 was also identified.30 GluK2 showed a larger molecular mass shift after treatment with EndoH, which indicates a larger immature N-glycan on GluK2 in the disorder. The gene discussed is SLC1A2; the disease is schizophrenia.