Finally, IL-1β can induce further expression of IL-1β[50,51], which could provide a powerful amplification mechanism to drive neuroinflammatory changes in the brain[13], and it can induce the expression of AQP4 in astrocytes[52], which could increase the amount of target molecules for pathogenic NMO-IgG. The gene discussed is IL1B; the disease is neuromyelitis optica.