In conclusion, the results from our in vivo and in vitro analysis did not reveal differences in any of the examined parameters addressing atherosclerotic plaque formation in p38αMY-KO/ApoE−/− mice compared to ApoE−/− controls, suggesting that p38α signaling in macrophages does not play an important role in the development of atherosclerosis in the ApoE deficient mouse model. This evidence concerns the gene APOE and atherosclerosis.