The specific manifestations of ALI are the increase of pro-inflammatory cytokines such as tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and interleukin-1β (IL-1β), as well as the release of other mediators caused by cascade amplification, resulting in increased pulmonary capillary permeability, interstitial edema, neutrophil exudation and a series of inflammation [5,6]. The gene discussed is IL1B; the disease is acute respiratory distress syndrome.