In an ApoE−/− mouse model, M2-like macrophages that internalized miR-let-7 attenuated atherosclerosis [56], whereas the opposite occurred when miR-33 was internalized by macrophages; miR-33 increased M1-like macrophage gene expression and upregulated endothelin-1 (ET-1) expression, promoting atherosclerosis in ApoE−/− mice [57]. Here, APOE is linked to atherosclerosis.