In the model of ALI, LPS engages the TLR4/NF-kB pathway inducing inflammation and neutrophil recruitment to the lungs, activating them to produce reactive oxygen species, increase the expression of adhesion proteins such as integrin (CD18), as well as the production of cytokines, such as TNF-a, IL-1β, IL-6, and the release neutrophil extracellular traps (NETs—free DNA, myeloperoxidase, histone), promoting diffuse alveolar damage and, consequently, difficulty in gas exchange [5]. The gene discussed is NFKB1; the disease is acute respiratory distress syndrome.