ARDS has long been recognized as a devastating complication of sepsis (19); it develops because sepsis can initiate a systemic inflammatory response that releases proinflammatory cytokines such as interleukin 6 (IL-6), IL-1β, IL-8, and tumor necrosis factor, and high levels of these cytokines can damage the alveolar-capillary barrier and alveolar type II cells (20, 21). The gene discussed is IL6; the disease is acute respiratory distress syndrome.