Major components of ARDS pathogenesis include the breakdown of cytotoxic mechanisms, over-activation of cytotoxic lymphocytes and macrophages with the excessive release of proinflammatory cytokines (IL-1, IL-2, IL-6, IL-8, IL-10, granulocyte colony-stimulating factor, and monocytic chemoattractant protein 1, MCP-1), inflammatory markers (CRP, serum ferritin), and infiltration of organs and tissues by activated T-lymphocytes and macrophages, causing hyperinflammatory reactions. The gene discussed is CCL2; the disease is acute respiratory distress syndrome.