Lung endothelial barrier dysfunction is both a cause and a consequence of severe lung inflammatory disease, including the lethal acute respiratory distress syndrome (ARDS).1Indeed, P53 expression levels are crucial for the integrity of the lung microvasculature, since P53 reduction due to LPS-induced P53 phosphorylation or small interfering ribonucleic acid has been previously shown to be related to the collapse of the lung barrier function.6Lipoteichoic acid (LTA) contributes in ARDS.7 The gene discussed is TP53; the disease is acute respiratory distress syndrome.