However, it has been reported that in NMO, anti-AQP4 IgG reduces glutamate uptake by astrocytes through down-regulation of the expression of excitatory amino acid transporter 2 (EAAT2), which is responsible for most of the glutamate uptake in the CNS (Hinson et al., 2008), raising the possibility that perturbation of glutamate homeostasis may contribute to myelin pathology in NMO (Marignier et al., 2010). This evidence concerns the gene AQP4 and neuromyelitis optica.