Inhibition of CXCL1 signaling through CXCR2 by the use of anti-CXCR2 antibodies or pharmacological antagonists had beneficial effects for in vivo models of demyelination and encephalomyelitis, such as reduced size of lesions, increased OPC differentiation, functional improvement, enhanced myelination, and reduced lesion load. The gene discussed is CXCR2; the disease is encephalomyelitis.