The evidence supports the above-mentioned hypothesis, including the following: higher AQP4-IgG levels in serum than in the CSF, the small number of T lymphocytes in NMO lesions, NMO-like lesions in nude (lack of T cells) mice, the harmful effect of natalizumab (the antibody inhibiting CNS entry of T cells, but not neutrophils) in some NMO patients and the possibility of NMO lesions formation in patients after fingolimod treatment, which acts mainly by inhibiting T lymphocyte egress from peripheral lymph nodes [9]. Here, AQP4 is linked to neuromyelitis optica.