In this context, biological biomarkers associated with endothelial damage (i.e., angiopoietin-2, intracellular adhesion molecule-1), epithelial cell damage (i.e., soluble receptor for advanced glycation and products, surfactant protein-D), inflammation (i.e., interleukin [IL], tumor necrosis factor-α [TNF-α]), and coagulation (i.e., protein C, plasminogen activator inhibitor-1, fibrinogen, D-dimer) have been described [39, 40] and associated with different subphenotypes of ARDS, which may partially explain why some pharmacologic therapies for ARDS have failed to improve patient outcomes [41]. This evidence concerns the gene TNF and acute respiratory distress syndrome.