Astrocyte-specific inhibition of NF-κB activation has been shown to dramatically ameliorate immune infiltration and tissue damage in experimental autoimmune encephalomyelitis (EAE), an animal model of MS, suggesting that genetic modulation of NF-κB signaling may alter astrocyte responses and astrocyte-mediated MS lesion pathology9,10. Here, NFKB1 is linked to experimental autoimmune encephalomyelitis.