Clinical studies suggested AQP4-IgG pathogenicity through different ways: high CSF AQP4-IgG titers and activated complement compounds during disease activity, high efficacy of treatments whose mechanisms of action reduced B cells and antibody levels, and the predilection of lesions in areas with high AQP4 expression.3, 22Furthermore, other studies have indicated that antibody positivity in patients with ON or extensive myelitis was associated with recurrent NMOSD attacks.28, 29. Here, AQP4 is linked to myelitis.