Although the mechanisms underlying the beneficial therapeutic effects of IFNβ on relapsing-remitting MS are still largely unknown, recent studies have indicated that IFNβ and type I IFN receptor-mediated signaling limit CNS autoimmunity by regulating innate immune responses in peripheral tissues [44,45] and the production and properties of TH17 cells, a pathogenic T helper subset largely responsible for CNS autoimmunity [46]. Here, IFNB1 is linked to relapsing-remitting multiple sclerosis.