Endothelial inflammation induced by thrombin, whose levels are elevated in the BALF of patients suffering from ALI [52], [53], is abolished upon BiP depletion as noted by inhibition of IKKβ-mediated phosphorylation and degradation of IκBα, an event responsible for the release and subsequent activation of NF-κB. This evidence concerns the gene NFKBIA and acute respiratory distress syndrome.