However, in the inflamed CNS of rats with NMO/EAE, such NMO patient-derived antibodies gain access to the CNS, find their cellular targets, fix and activate the classical complement cascade[3,4] and trigger the formation of granulocyte-rich, astrocyte-destructive lesions[3-5,11] similar to what is seen just after the direct injection of NMO patient-derived AQP4 specific antibodies and human complement into the mouse brain[12]. This evidence concerns the gene AQP4 and neuromyelitis optica.