In particular, we suspect glutamate as a candidate for alterations in NMO because glutamate transporters GLT1/EAAT2 and GLAST/EAAT1 coexist extensively with AQP4 at astrocyte membrane, and a functional link between AQP4 and GLT1 has been reported [43]; AQP4 and GLT1 are downregulated in CNS lesions of NMO patients [13]; and finally, contact with AQP4-IgG leads to GLT1 endocytosis [8, 13] and maintains its sequestration into the cytoplasmic compartment (our data herein). The gene discussed is SLC1A2; the disease is neuromyelitis optica.