In ApoE-deficient mice, expression of transgenic ApoE, an essential component of serum high density lipoproteins (HDL) and triglyceride-enriched lipoproteins that possess atheroprotective properties, negatively regulates miR-221/222 and restores p27Kip1 expression in VSMCs thereby preventing pathological recruitment of these cells in atherosclerosis-related vascular remodeling. Here, APOE is linked to atherosclerosis.