NFKB1 and serum lipopolysaccharide activity: Inhibition of endothelial NFκB signaling by overexpression of a degradation-resistant form of the NF-κB inhibitor I-κBα under the control of the endothelial cell specific VE-cadherin-5 promoter attenuated tissue inflammation and organ injury during endotoxemia and abdominal sepsis [16]–[19].