Since cerebral ischemia induces innate immune responses and NF-κB is a regulator of innate immunity, agents that modulate the activity of NF-κB may modulate the inflammatory process in ischemic stroke, suggesting that TLR4 activation is associated with the expression and activation of proinflammatory cytokines of the NF-κB signaling pathway [33,34,35,36,37]. This evidence concerns the gene NFKB1 and ischemic stroke.