All the evidence summarized above strongly suggests that the IL-1β released in NMO lesions and the IL-1β-induced local production/accumulation of complement components might facilitate neutrophil entry and BBB breakdown in the vicinity of NMO lesions, and might thus be an important secondary factor for lesion formation, possibly by paving the ground for rapid lesion growth and amplified immune cell recruitment to this site. The gene discussed is IL1B; the disease is neuromyelitis optica.