End-stage bacterial/viral infections induce an excessive and unusual host immune response, often accompanied by excessive production of inflammatory cytokines, such as interleukin-2 (IL-2), IL-6, IL-7, granulocyte colony-stimulating factor, interferon gamma-induced protein 10, monocyte chemotactic protein 1, macrophage inflammatory protein 1 alpha, and tumor necrosis factor α (TNF-α), resulting in pulmonary edema and subsequent acute lung injury/acute respiratory distress syndrome (ALI/ARDS) [1]. This evidence concerns the gene CCL3 and acute respiratory distress syndrome.