Our data also suggest that although other local factors (i.e. complement activators/inhibitors) may contribute to the tissue‐specific damage of NMO‐IgG, differences in AQP4 suprastructure are per se sufficient to explain the absence of skeletal muscle damage and provide a rationale as to why the effect is mainly in the CNS. This evidence concerns the gene AQP4 and neuromyelitis optica.