The pathogenesis of ALI/ARDS includes an acute phase characterized by initial damage to the vascular endothelium and/or alveolar epithelium resulting in increased alveolar and capillary permeability and pulmonary edema, neutrophil accumulation, the release of proinflammatory cytokines including TNF-α, IL-1β, and IL-6, and the release of toxic proteases and reactive oxygen species [75]. The gene discussed is IL1B; the disease is acute respiratory distress syndrome.