In addition, researchers transfected NOX4 siRNA in CLP-induced ALI mice and found that NOX4 knockdown inhibited the activation of the CaMKII/ERK1/2/MLCK oxidation pathway, restored the expression of tight junction proteins ZO-1 and occludin in the pulmonary endothelial cells of mice, and maintained the integrity of the pulmonary endothelial cell barrier. This evidence concerns the gene NOX4 and acute respiratory distress syndrome.