A recent study using, a mouse model of intrauterine infection showed that the TLR signaling induced preterm labor, which was mediated by activation of the NF-κB pathway [12, Furthermore, mice with MyD88 knockout showed improved LPS-sensitized hypoxic ischemic-induced brain injury, and this protective effect was likely mediated by reduced NF-κB activation and attenuated pro-inflammatory cytokine and chemokine production [13]. Here, NFKB1 is linked to injury.