MR16-1 inhibited STAT3 activation and development of atherosclerotic lesions in both IκBNS−/−/LDLr−/− and LDLr−/− mice, suggesting IL-6 is a main contributor to atherogenesis, and inhibition of IL-6 might be a new method to prevent the development of atherosclerosis. Here, STAT3 is linked to atherosclerosis.