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WELL-DEVELOPED LESIONS of atherosclerosis have substantial amounts of lipid underlying them and cholesterol is present in this fatty debris. These facts fastened attention of early investigators on this substance and led to the supposition that cholesterol is a major factor in the evolution of the disease process. This assumption was strengthened by the production, in animals, of superficially similar lesions by dietary manipulations causing increased levels of blood cholesterol. Taken together with the apparent relationship of coronary disease and dietary lipid intake in different geographical and ethnic groups, investigators have been encouraged in their belief in the "insudation" concept of the origin of atherosclerosis. 1 There is no serious question of the fact that the main lesion of human atherosclerosis is a cellular proliferation, the fibrous plaque, and the prime cell comprising the lesion is a form of smooth muscle cell. Recent proposals concerning the pathogenesis of atherosclerosis have modified the older hypothesis to include the proliferative component." 2 -One suggestion has been that lipoproteins, since they seem to be preferred nutrients for the arterial medial cells, by their delivery in excess of usual amounts through damaged endothelium, stimulate arterial wall cell proliferation. The assumption in this and similar formulations is that the medial cells, as such, are the proliferating cells. Comparison of the naturally-occurring atherosclerotic plaques of human beings and birds with the reparative response of mammalian aorta to injury3' 4 led us to consider an alternative to the injury-repair hypothesis currently in vogue. This was based upon the following considerations: Cells of spontaneous lesions differ from cells of normal arterial wall media and also from cells populating a repair site. They differ in size and arrangement of cells, in composition

Evidence for a Monoclonal Origin of Human Atherosclerotic Plaques and Some Implications