Of the various hypotheses offered to explain atherosclerosis, inflammation now appears to provide a key to this pathological process. Inflammation has been shown to play a major role in precipitating a cascade of events from formation of the atheromatous lesion in response to vascular injury through lipid ingestion by macrophages, to subsequent rupture of the lesion, and myocardial infarction. Atherosclerosis shares many inflammatory features with rheumatoid arthritis (RA), an autoimmune disease, and drugs that block the inflammatory cytokine pathway now provide effective treatment for RA. In animal models, blockers of the inflammatory cytokine pathway appear to block mononuclear cell binding to arterial plaque. C-reactive protein (CRP), an inflammatory marker, may also play a proinflammatory role in activating monocyte chemotactic protein. Antiatherosclerotic drugs may be exerting some of their beneficial effects by inhibiting the harmful effects of CRP.