The critical observations that leukocyte-specific 11βHSD1 deficiency reduces plaque burden and in vivo cholesterol accumulation in peritoneal macrophages is reduced in 11β−/−/apoE−/− mice suggest that inhibition of 11βHSD1 can modulate an important function of the macrophage central to atherosclerosis pathophysiology. This evidence concerns the gene APOE and atherosclerosis.