Hypercholesterolemia in apoE-deficient mice leads to the expansion of Ly-6C high (Ly-6C $^{hi}$) monocytes, which contribute to atherosclerosis by accumulating in atherosclerotic lesions and differentiating into macrophages. This study shows that Ly-6C $^{hi}$ monocytes increase dramatically in hypercholesterolemic apoE-deficient mice on a high-fat diet, with their numbers doubling every month. These monocytes adhere to activated endothelium, infiltrate atherosclerotic lesions, and become lesional macrophages. Hypercholesterolemia-associated monocytosis (HAM) is driven by increased survival, continued proliferation, and impaired conversion of Ly-6C $^{hi}$ to Ly-6C $^{lo}$ monocytes. Statin treatment reduces HAM by lowering cholesterol levels and decreasing Ly-6C $^{hi}$ monocyte numbers. Ly-6C $^{hi}$ monocytes are more likely to accumulate in atherosclerotic lesions than Ly-6C $^{lo}$ monocytes, and their presence is associated with increased atherosclerosis. These findings suggest that Ly-6C $^{hi}$ monocytes are key mediators of chronic inflammation in atherosclerosis and that their expansion is linked to hypercholesterolemia. The study also highlights the role of CCR2 in monocyte recruitment to atherosclerotic lesions, as CCR2-deficient mice show reduced atherosclerosis. Overall, the study provides new insights into the mechanisms of atherosclerosis and the role of Ly-6C $^{hi}$ monocytes in the inflammatory process.Hypercholesterolemia in apoE-deficient mice leads to the expansion of Ly-6C high (Ly-6C $^{hi}$) monocytes, which contribute to atherosclerosis by accumulating in atherosclerotic lesions and differentiating into macrophages. This study shows that Ly-6C $^{hi}$ monocytes increase dramatically in hypercholesterolemic apoE-deficient mice on a high-fat diet, with their numbers doubling every month. These monocytes adhere to activated endothelium, infiltrate atherosclerotic lesions, and become lesional macrophages. Hypercholesterolemia-associated monocytosis (HAM) is driven by increased survival, continued proliferation, and impaired conversion of Ly-6C $^{hi}$ to Ly-6C $^{lo}$ monocytes. Statin treatment reduces HAM by lowering cholesterol levels and decreasing Ly-6C $^{hi}$ monocyte numbers. Ly-6C $^{hi}$ monocytes are more likely to accumulate in atherosclerotic lesions than Ly-6C $^{lo}$ monocytes, and their presence is associated with increased atherosclerosis. These findings suggest that Ly-6C $^{hi}$ monocytes are key mediators of chronic inflammation in atherosclerosis and that their expansion is linked to hypercholesterolemia. The study also highlights the role of CCR2 in monocyte recruitment to atherosclerotic lesions, as CCR2-deficient mice show reduced atherosclerosis. Overall, the study provides new insights into the mechanisms of atherosclerosis and the role of Ly-6C $^{hi}$ monocytes in the inflammatory process.