These studies used ApoE-deficient mice in which the ApoE- deficiency causes severe accumulation of cholesterol in macrophages resulting in a high pro-inflammatory state, which could explain the differences observed in atherosclerosis development between our low grade inflammation model of E3L.CETP mice fed a low amount of dietary cholesterol (twice human daily intake) [32], [33]. Here, APOE is linked to atherosclerosis.