In contrast to classical ApoE−/− and LDLr−/− mice, ApoE−/−Fbn1C1039G+/− mice develop advanced atherosclerotic plaques with IP angiogenesis and hemorrhage in the carotid artery [14, 15], which is obviously required to tackle erythrophagocytosis-induced effects in atherosclerosis in vivo. Here, APOE is linked to atherosclerosis.