Early rat models involved administration of AQP4-IgG following induction of experimental autoimmune encephalomyelitis (EAE) [4]; however, the pathogenic mechanism in EAE – myelin targeting by T cells – is very different from the humoral immune response in NMO, making it difficult to reach conclusions about NMO pathogenesis mechanisms. Here, AQP4 is linked to neuromyelitis optica.