At high concentrations, the role of TNF in the regulation of lung function during pneumonia, ARDS and lung transplantation is traditionally thought to be mainly deleterious, mediated by TNF-TNFR1 signaling and characterized by increased alveolar epithelial and capillary endothelial cell demise, impaired AFC, barrier dysfunction, oxidative stress and hyper-inflammation. The gene discussed is TNF; the disease is acute respiratory distress syndrome.