This model of disease is supported by two reports of passively transferred NMO-IgG in which the NMO-IgG exacerbates behavioral signs of rat experimental autoimmune encephalomyelitis (EAE) and induces a pathology similar to human NMO: areas of acute inflammation with granulocytes, a dramatic loss of aquaporin-4 staining and complement deposition [5,6]. The gene discussed is AQP4; the disease is neuromyelitis optica.