Evidence for an important role of complement in seropositive NMO includes vasculocentric deposition of activated complement in NMO-affected human tissues [2, 10–12], complement-dependent NMO pathology in rodents following passive transfer of AQP4-IgG [13–15], and efficacy of the C5 complement inhibitor eculizumab in a preliminary clinical trial [16]. The gene discussed is C5; the disease is neuromyelitis optica.