Our current understanding of the vascular biology of atherogenesis and its clinical manifestations suggests a pathophysiology that is much more complex than mere lipid storage. Recent advances support the current view of atherosclerosis as an inflammatory process that initiates and promotes lesion development to the point of acute thrombotic complications and clinical events. Inflammatory cells localize in early-stage atherosclerotic lesions, and recent basic research has established a causal relation between inflammatory mediators or cytokines, and the steps involved in progressing from local inflammation through plaque formation. Inhibition of the action of certain specific proinflammatory cytokines, such as CD40 ligand, interferes with atherogenesis in mice. Increased circulating levels of inflammatory markers indicate increased cardiovascular risk. Thus, the time has come to embrace inflammation as a common pathway for atherogenic risk factors and for providing new opportunities for therapeutic intervention.