Recent experimental evidence indicates that all the lesions seen in human atherosclerosis can be induced in animals by various forms of injury to the intima or endothelial lining of arteries. Dietary lipid supplement is not required for the development of lipid-rich atherosclerotic lesions in these settings. Factors present in plasma or serum may stimulate the proliferation of smooth muscle cells in the lesions similar to the invitro demonstration of smooth muscle cell proliferation in response to diabetic serum. The accumulation of lipid in lesions may relate to alteration in the glucosaminoglycan content of the neointima covered by regenerated endothelium and may be analagous to alterations in glucosaminoglycan metabolism in the arterial wall of diabetic subjects.