ARDS pathological findings such as pulmonary edema of non-cardiogenic origin, dyspnea, increased inflammatory mediators, such as cytokines (TNF-α, IL-6, and IL-8) and chemokines/receptors (CXCL-1, CXCL-8, and CXCR4), migration of inflammatory cells to the tissue, and intra-alveolar space, as well as increased capillary alveolar permeability, are key the disease pathogenesis [8–10]. The gene discussed is TNF; the disease is acute respiratory distress syndrome.