Several lines of evidence suggest that the Fas/FasL system plays a role in ALI/ARDS. First, bioactive sFasL is present in the lungs of patients with ARDS, and this is associated with increased mortality [9, 12] . Second, genetic variations in the Fas gene are associated with increased risk for ALI/ARDS in humans [13] . Third, activation of the Fas/FasL system in mammals leads to acute inflammatory injury followed by fibrosis [14] [15] [16] [17] . And finally, mice lacking Fas are protected in a number of models of lung injury [11, [18] [19] [20] . Thus, the apoptotic and inflammatory responses induced by Fas activation in the lungs are one important factor in the development of ALI/ARDS.