This is corroborated by the finding, that both defective IL-1β signaling [45] as well as TNF-α signaling [46] resulted in decreased chemokine upregulation and attenuated neutrophil infiltration and that in a selection of patients with episodes of ischemia/reperfusion (major blunt trauma, ruptured aortic aneurysm) increased levels of TNF-α, IL-1β and IL-8 are associated with increased mortality and increased risk for acute respiratory distress syndrome and multi-organ failure [47,48]. The gene discussed is IL1B; the disease is acute respiratory distress syndrome.