Thus, septic pulmonary microvascular/PMVEC dysfunction including high-albumin pulmonary edema and enhanced PMN sequestration, key pathophysiologic features of septic ALI, appear to be the result of PMVEC death specifically due to caspase-dependent apoptosis, which appears to be mediated through the activity of both iNOS and NADPH oxidase. The gene discussed is FMO5; the disease is acute respiratory distress syndrome.