Our own experiments with the Fas and FasL mutant mice showed a marked decrease in inflammation in the lungs of these animals in response to hemorrhageinduced septic ALI, when compared to background animals (132) . This phenomenon also was evident following Fas silencing in the mouse lungs using siRNA (152) and was associated, in both cases, with a reduction of PMN immigration into the lungs (132, 152) . Further experiments revealed that lung epithelial cells were capable of secreting MIP-2, KC, and MCP-1 in vitro in response to Fas activation, through mechanisms involving ERK and, potentially, FLIP (132), complementing the findings of other researchers who demonstrated that a NF-κB dependent mechanism appears to underlie this response (151) . Instillation of a Fasactivating antibody into transgenic murine lungs in which lung macrophage numbers are markedly reduced displayed a similar inflammatory response as seen in background animals, further supporting a role for Fas-mediated, ep- ithelial cell-induced pulmonary inflammation in vivo (132) . The fact, that inhibition of Fas activation modulated both PMN recruitment into the lung as well as pulmonary epithelial apoptosis, intriguingly points at its value as a potential therapeutic target in ALI.