Interestingly, in addition to mechanical stimulation, ENaC can also be activated by reactive oxygen species (ROS) [79], which are generally increased in ALI/ARDS lungs [80–82], For instance, in an LPS-induced ALI/ARDS model, LPS can stimulate ROS production by activating the NADPH oxidase 2/Rac1 pathway, and elevated ROS increased ENaC activity and enhanced AFC capacity [80], indicating that ROS-induced enhancement of ENaC activity may be a protective mechanism to counteract edema formation during the exudative phase of ALI/ARDS. This evidence concerns the gene RAC1 and acute respiratory distress syndrome.