The pathogenesis of acute lung injury (ALI) is attributed to an excessive inflammatory response leading to the destruction of lung tissue, which is manifested as tumor necrosis factor-necrosis alpha (TNF-α) induction by various cytokines, the increased expression of interleukin-1 (IL-1), and an inflammatory cascade mediated by cytokines, which aggravates lung tissue injury. The gene discussed is TNF; the disease is acute respiratory distress syndrome.