Genetic knockout of CCR2 (CCR2−/−) in the Apolipoprotein E-deficient (apoE−/−) mouse model of atherosclerosis resulted in a significant decrease in lesion size compared to apoE−/− controls, which was caused by a reduction in monocyte/macrophage recruitment to the atherosclerotic lesion4–6. The gene discussed is APOE; the disease is atherosclerosis.