The fact that 10–25% of NMO patients are AQP4-IgG-seronegative provides that the immunopathogenesis of the disease is heterogeneous and may involve other factors, such as antibodies against myelin oligodendrocyte glycoprotein (MOG-IgGs) and autoantibodies against aquaporin-1 (AQP1-IgGs) [58]. This evidence concerns the gene MOG and neuromyelitis optica.