Other studies of the alveolar-capillary barrier have shown that tight and adherens junctions are important in maintaining alveolar permeability, with claudin-18 knockouts showing increased paracellular alveolar permeability [24, 25] and loss of vascular endothelial cadherin (VE-cadherin) implicated as a major mechanism of increased permeability in acute respiratory distress syndrome (ARDS) [26]. The gene discussed is CLDN18; the disease is acute respiratory distress syndrome.