Endotoxin binds Toll-like receptor (TLR)-4 on macrophages, endothelium, airway, and alveolar epithelium (type I and II), leading to the production of chemokines and pro-inflammatory cascade, such as tumor necrosis factor (TNF)-α and interleukin-1β, which might be crucial in the ALI pathogenesis [2,3]. The gene discussed is TNF; the disease is acute respiratory distress syndrome.