Existing mouse models of NMO rely on the concurrent initiation of active (via immunization) or passive (via transfer of myelin-specific T cells) EAE [44–46], co-injection of NMO IgG and human complement factors into the CNS [47–49], or injection of the proinflammatory cytokine IL-1β directly into the brain to drive granulocyte recruitment and complement factor production [50]. The gene discussed is IL1B; the disease is neuromyelitis optica.