We found that a lipid inhibitor (MJ33) of aiPLA2 activity or its genetic inactivation were effective in modulating LPS-induced or hyperoxia-mediated ALI in mice, providing evidence that aiPLA2 and subsequent NOX2 activation plays an important role in ALI, at least in mice [22,23,24,25,26]. This evidence concerns the gene PRDX6 and acute respiratory distress syndrome.