CARDIOVASCULAR disease remains the chief cause of death in the United States and Western Europe, and atherosclerosis, the principal cause of myocardial and cerebral infarction, accounts for the majority of these deaths.¹ This review, like its predecessor,² will not attempt to cover all literature on atherosclerosis. In a previous review of the pathogenesis of atherosclerosis,² Glomset and I discussed various hypotheses of atherogenesis^{2 3 4 5 6 7} and emphasized the importance of intimal smooth-muscle proliferation as the key event in the development of the advanced lesions of atherosclerosis. The response-to-injury hypothesis of atherogenesis^{2 3 4 5 6} proposes that "injury" to the endothelium is the initiating event in . . .