Inactivation of NFATc1 in B cells led to an increase in IL-10 production and amelioration of symptoms of MOG-mediated experimental autoimmune encephalomyelitis21, and inactivating both Nfatc1 and Nfatc2 genes in T cells abolished the generation of experimental autoimmune encephalomyelitis symptoms53. The gene discussed is NFATC1; the disease is experimental autoimmune encephalomyelitis.