The author summarized that lung barrier dysfunction during ARDS results from the death of alveolar epithelial and pulmonary endothelial cells, which can be triggered by apoptosis pathways such as FasL, TNF-α/TNFR1, and TNF-related apoptosis-inducing ligand (TRAIL) signaling events. This evidence concerns the gene TNFRSF1A and acute respiratory distress syndrome.