Recruitment of mononuclear leukocytes and the migration, growth, and activation of the multiple cell types within atherosclerotic lesions are critical features of the chronic inflammatory and fibroproliferative response central to atherosclerosis. Attraction of leukocyte to tissues is controlled by chemokines, whose presence is well documented in atherosclerotic lesions. Studies using knockout and transgenic murine models have demonstrated that chemokine receptor/ligand interactions are of crucial importance in the development of atherosclerosis. Beyond their chemotactic effect on mononuclear leukocytes, chemokines may also interfere with smooth muscle cell migration and growth, as well as platelet activation and other well-defined features of the atherosclerotic process. There is no doubt that the identification of chemokines as important vascular signals has provided insights into our understanding of basic cellular and molecular mechanism of atherosclerosis. Thus, there is evidence that chemokine receptor/ligands could be identified as potential new targets for therapeutic intervention to prevent or control atherosclerosis in the near future.