The pathological mechanism involves the binding of AQP4-IgG to anti-aquaporin-4 (AQP4) water channels on astrocyte foot processes, triggering complement cascade activation, resulting in astrocyte damage and subsequent secondary injury to oligodendrocytes and neurons (2).According to the revised criteria published by Wingerchuck et al., a positive AQP4 antibody with the presence of a single core clinical feature (optic neuritis, acute myelitis, or brainstem syndrome) is sufficient for diagnosis once other diseases have been ruled out (3). Here, AQP4 is linked to optic neuritis.