These included: (a) BTK, involved with neutrophil and macrophage response in infection-induced ARDS such as influenza28, SARS-CoV-229 and LPS/immunocomplex30, promotes a pro-inflammatory neutrophilic response through TLR4 signaling30; and (b) STAT1, an interferon-induced stimulator with function in CCL5 and CXCL11 regulation31. This evidence concerns the gene CCL5 and acute respiratory distress syndrome.