The reason for this could be that the NMO-IgGs used in the animal models did not only contain AQP4-abs, but additionally other immunoglobulins, that the AQP4-abs found in NMO-IgG preparations were polyclonal, with differences in pathogenicity and affinities [7], that the human AQP4-abs suboptimally interact with rat complement [4], or that the animal studies just simply did not reach the perfect time window for CNS injury [4, 21, 40]. The gene discussed is AQP4; the disease is neuromyelitis optica.