The mechanistic role of HMGB1 in oxidative stress-induced ALI is incompletely understood; extracellular HMGB1, either actively secreted by immune cells or passively released by necrotic cells, has been implicated in the pathophysiology of a variety of inflammatory conditions (Scaffidi et al. 2002; Yang et al. 2001), such as sepsis and rheumatoid arthritis (Andersson et al. 2000; Taniguchi et al. 2003; Wang et al. 1999; Wang et al. 2004). This evidence concerns the gene HMGB1 and acute respiratory distress syndrome.