A few important observations support this notion, including: the colocalization of immunoglobulin with a marker of the terminal lytic complement complex (C9neo antigen), the presence of activated macrophages and significant vascular hyalinization in perivascular regions in active NMO lesions [56], and in vitro experiments which demonstrate the colocalization of AQP4 with EAAT2, a glutamate transporter and the fact that AQP4 and EAAT2 were endocytosed in the presence of NMO-IgG [59]. Here, SLC1A2 is linked to neuromyelitis optica.