Much evidence has shown that the exposure of ECs to LPS, a Gram-negative bacterial product, can result in endothelial dysfunction (the increased expression of adhesion molecules and chemokines) and inflammatory response (the increased expression of iNOS and pro-inflammatory cytokines) through the activation of NF-κB signaling pathway [39,40,41]. The gene discussed is NFKB1; the disease is endothelial dysfunction.