A recent study using ApoE−/− mice demonstrated that the secondary granule protein CAMP, a known C/EBPε target gene, directly promotes atherosclerosis by enhancing recruitment of inflammatory monocytes [23] Another study using the ApoE−/− murine model reported that neutropenic mice had reduced plaque sizes at early but not late stages of atherosclerotic lesion formation, suggesting an important role of neutrophils in the initiation of atherosclerosis [24]. This evidence concerns the gene APOE and atherosclerosis.