A new mouse model of NMO has been established that utilizes continuous infusing of AQP4-specific IgG into the spinal subarachnoid space, without exogenous complement (70). Recipients of monoclonal AQP4-IgG or NMO-patient-derived IgG displayed progressive motor impairment and immunohistopathology compatible to early clinical NMO pathology. This evidence concerns the gene AQP4 and neuromyelitis optica.