A previous study showed that blocking CXCR2, the main receptor of CXCL1 and CXCL2, effectively decreased alveolar accumulation of neutrophils in the CLP model of sepsis [4], demonstrating that CXC chemokines are important regulators of pulmonary infiltration of neutrophils in septic lung injury. The gene discussed is CXCR2; the disease is Sepsis.