The cellular characteristics of ALI include excessive transepithelial neutrophil migration into the alveolar and interstitial spaces, loss of alveolar–capillary membrane integrity, the release of pro-inflammatory and cytosolic mediators such as interleukin (IL-6), IL-1β, and tumor necrosis factor (TNF), and upregulation of nuclear factor kappa B (NF-κB) and mitogen-activated protein kinases (MAPK) signaling pathways [11,12]. The gene discussed is NFKB1; the disease is acute respiratory distress syndrome.