Evidence suggests that CXCL1, and particularly CXCL2, are the key mediators of neutrophil migration early after focal brain injury, with both CXCL1 and CXCL2 found to be acutely upregulated within 5 h of experimental cortical impact injury in both mice and rats [61, 104], while after lateral fluid percussion injury CXCL2 expression has been shown to peak at 4 h in the injured hemisphere [105]. The gene discussed is CXCL2; the disease is injury.