During ALI, excessive ROS generation contributes to the endothelial and epithelial barrier disruption, resulting in leakage of fluids into the pulmonary parenchyma and massive leukocyte (e.g., neutrophils and macrophage) infiltration, as well as robust pro-inflammatory mediator production such as IL-6, TNF-α and IL-8 [1, 33, 34]. The gene discussed is IL6; the disease is acute respiratory distress syndrome.