In patients with ARDS, neutrophil infiltration into the lungs is further augmented by a compromised alveolar-capillary barrier brought about by the action of proinflammatory mediators.32 Consistent with previous reports,17 18 33 we showed that TNF-α contributed to increased endothelial permeability and found that GSK1995057 prevented this increase, suggesting that TNFR1 signalling (rather than TNFR2 signalling) mediates TNF-induced endothelial permeability. Here, TNFRSF1B is linked to acute respiratory distress syndrome.