The upregulation of TGF-β in ARDS causes an ENaC trafficking defect with a marked reduction in the cell-surface abundance of ENaC on lung epithelial cells, thereby rapidly and substantially impairing the alveolar fluid reabsorption in ARDS patients and contributing to the persistence of their pulmonary edema (Peters et al., 2013). The gene discussed is TGFB1; the disease is acute respiratory distress syndrome.