A growing body of experimental evidence suggests that in addition to the injury caused by high tidal volumes, even moderate or low tidal volumes markedly enhance injury when the lungs are exposed to pathogens or their products [4] [5] [6] . For example, mechanical ventilation synergistically enhances lung injury in response to low doses of bacterial lipopolysaccharide (LPS) and this is associated with expression of specific sets of genes that aren't expressed with LPS or ventilation alone [4, 5, 7] . A computational analysis has mapped the biological processes that are activated by the combination of mechanical ventilation and LPS [8] . One of these biological processes is apoptosis, and a known mediator of apoptosis in injured lungs is the Fas/FasL system.