CD11c+ myeloid cells are present in the arterial wall at athero-susceptible sites exposed to alterations in hemodynamic stress, such as curvatures and bifurcations.25 CD11c expression by monocytes is upregulated by hypercholesterolemia,26 and depletion of CD11c+ cells has been shown to reduce atherogenesis in ApoE-/- mice.19,26 Collectively, these studies indicate the existence of proatherogenic CD11c+ myeloid cell populations. This evidence concerns the gene APOE and familial hypercholesterolemia.