Atherosclerosis is no longer considered a disorder due to abnormalities in lipid metabolism. In fact, the inciting event of atherosclerosis is likely an inflammatory insult that occurs decades before the disease becomes clinically apparent. Rapidly evolving knowledge of the pathogenesis of atherosclerosis, coupled with novel, target-specific therapies, is revolutionizing the treatment of atherosclerosis. As a result, a variety of treatments are now undergoing evaluation for their ability to ameliorate the inflammatory pathways likely to cause the atherosclerotic process to initiate and propagate. Once initiated, atherosclerosis progresses as a result of a well-studied series of changes in the constituent cellular make-up of the vessel wall. Specific cytokine-mediated events in this cycle are required for lesional growth. The clinical manifestations of atherosclerosis occur so late in this process that interventions such as percutaneous coronary interventions can deal with isolated areas of disease; however, they do not influence the underlying disease process.