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. Here, TNFRSF1A is linked to pneumonia.