GFAP and neuromyelitis optica: NMO–IgG/AQP4–IgG is thought to mediate pathogenesis by binding selectively to AQP4 on CNS astrocytes, causing complement fixation, generation of chemotactic signals (e.g., C3a, C5a), immune cell infiltration, and subsequent loss of AQP4 and glial fibrillary acidic protein (GFAP) on the astrocytes (2).