Increased NF-κB activation in Nrf2−/− mice when compared with wild-type after stimuli such as traumatic brain injury [25], LPS [8], TNFα [8], ovalbumin [7], and respiratory syncytial virus [26] was observed. In vivo and in vitro data suggest that many Nrf2 activators confer protective effect against oxidative stress and inflammatory response through suppressing NF-κB signal activation. This evidence concerns the gene NFKB1 and injury.