In vivo models have demonstrated that intratracheal or intranasal administration of HMGB1 caused ALI, which has been reflected by enhanced acute inflammatory injury to the lungs, neutrophil accumulation, development of lung edema, and increased pulmonary production of IL-1β, TNFα, and macrophage-inflammatory protein (MIP)-2 [115, 116]. The gene discussed is HMGB1; the disease is acute respiratory distress syndrome.