NFKB1 and Sepsis: Experiments in transgenic mice overexpressing the IkB-α super-repressor in endothelial cells, have demonstrated that inhibition of the NFκB signaling pathway in LPS-stimulated mice causes a defect in expression of endothelial tight junction proteins, and as a result, a loss of integrity of the endothelium and increased vascular permeability [157], suggesting that NFκB is responsible for the stress-induced responses of the endothelium to septicemia or TNF-α.