While ROS and oxidative stress contribute to lung injury in many aspects, and various members of the MAPK family are involved in iNOS regulation, the ROS/p38 MAPK/NF-κB pathway may represent an essential signaling mechanism that mediates the pro-inflammatory role of neutrophils in ALI, e.g. release of nitroxides to permeabilize microvascular endothelial cells in the lung [37, 38]. This evidence concerns the gene NFKB1 and acute respiratory distress syndrome.