Herein, the authors demonstrated that IKK2-mediated inflammatory myeloid cell activation exacerbates experimental autoimmune encephalomyelitis by potentiating TH1/TH17 cell activation and decreased permeability of the blood brain barrier (BBB) indicating myeloid-IKK2 as a potential therapeutic target for treatment of MS [76]. Here, IKBKB is linked to experimental autoimmune encephalomyelitis.