Furthermore, the high airspace concentrations of Ang‐2 measured in human clinical samples of undiluted pulmonary edema fluid from patients with ARDS (Bhandari et al., 2006; Qi et al., 2016) and in the current work with influenza suggest that Ang‐2 may have previously unappreciated direct effects on epithelial barrier function, which may act synergistically with increased endothelial permeability to increase alveolar edema. The gene discussed is ANGPT2; the disease is acute respiratory distress syndrome.