While the present study was not designed to address the molecular mechanisms by which CXCR4 activation prevents ARDS development, several lines of evidence suggest that CXCR4 activation protects endothelial barrier function, and regulates vascular smooth muscle function and blood pressure through heteromerization with α1-adrenergic receptors9,11,34–37. This evidence concerns the gene CXCR4 and acute respiratory distress syndrome.