Although Ly6chi monocytes were reduced out to 6 months of age in CCR2-deficient dystrophic mice, myonecrosis and fibrosis returned to control levels by this point (69), suggesting that other monocyte or macrophage populations promote dystrophinopathy at later stages of disease. The gene discussed is CCR2; the disease is neuromuscular disease caused by qualitative or quantitative defects of dystrophin.