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A central regulator of inflammation, nuclear factor kappa B (NFkB), has been implicated as a driver of the autoimmune disease multiple sclerosis (MS). A team led by David Hafler, of the Ó³»­´«Ã½ and Yale School of Medicine, demonstrated that MS-associated variants alter NFkB signaling pathways, leading to increased activation of NFkB and making cells more responsive to inflammatory stimuli. The work, featured in , suggests that rapid genetic screening for variants associated with NFκB signaling may identify individuals amenable to therapeutics targeting this pathway.