It has been reported previously that bacterial endotoxin-challenged bronchial epithelial cells secrete high levels of CXCL8 and CXCL5 and that these act as autocrine agonists for these cells [8], and others have documented that vascular endothelial and alveolar epithelial cells expression of CXCR2 plays an important role in pulmonary pathology in models of LPS-induced pneumoniae in mice [20, 21]. The gene discussed is CXCL8; the disease is pneumonia.