The injection of a small dose of LPS in mice prior to MCAO was also able to generate tolerance to the subsequent cerebral ischemic damage, which was mainly dependent on the inhibition of TLR4 and the activation of the downstream signaling molecule NF-κB, thereby alleviating the inflammatory reaction of cerebral ischemia produced by this pathway [86]. This evidence concerns the gene NFKB1 and brain ischemia.