APOE and atherosclerosis: Mice lacking the glucocorticoid inactivating enzyme 11β-HSD2 display accelerated atherosclerosis development when crossed with ApoE−/− mice, compared to controls [67], while mice lacking the enzyme responsible for generating active corticosterone from inactive 11-dehydro corticosterone in tissues, namely 11β-HSD1, have reduced plaque size and severity on an ApoE−/− background compared to controls [68].