It regulates the pro-inflammatory activation of microglia by inhibition of overexpressed, activated Sur1-KATP channels after acute and chronic neuroinflammation [8,9]; improves the course of Experimental Autoimmune Encephalomyelitis (EAE), a multiple sclerosis model, by inhibiting up-regulated Sur1-Trpm4 channels in astrocytes [59]; and blocks NLRP3 inflammasome/IL-1β signalling by down-regulation of the release of pro-inflammatory cytokines and reactive oxygen species. This evidence concerns the gene IL1B and multiple sclerosis.