The protective effect against ALI (translated in less pulmonary edema and inflammation) seems to be associated with the increased lung expression of aquaporins (AQP) 1 and 5 (AQP1 in the alveolar capillary endothelial cells and AQP5 in the alveolar type I and II cells), transmembrane proteins dedicated to water transport, whose decrease is strongly coupled with the development of ALI and pulmonary edema) [111]. This evidence concerns the gene AQP1 and acute respiratory distress syndrome.