Jiang J et al. [21] confirmed that NOX4 knockdown attenuated the redox-sensitive activation of the CaMKII/ERK1/2/MLCK signal pathway, and restored the expression of tight junction proteins ZO-1 and occludin in lung endothelial cells to maintain the integrity of the barrier of endothelial cells, which suggested that targeting NOX4 is an innovative and effective treatment for ALI. This evidence concerns the gene NOX4 and acute respiratory distress syndrome.