For instance, recombinant growth-arrest-specific protein 6 reduced neuroinflammation after middle cerebral artery occlusion in rats by disrupting TLR-TRAF-NF-κB signaling at the level of TRAF (Wu et al., 2018), and a small molecule inhibitor of CD40–TRAF6 signaling was shown to reduce inflammation in rodent models of multiple sclerosis (Aarts et al., 2017). This evidence concerns the gene NFKB1 and multiple sclerosis.