Forty-five rhesus monkeys were divided into five groups fed four different high-fat diets and a stock diet. The duration of feeding varied from 33 to 70 weeks. All monkeys fed the high-fat diets developed aortic proliferative lesions composed predominantly of spindle-shaped cells, most of them laden with lipid. The thickest of these proliferative lesions measured 0.85 mm, and most were thinner, suggesting that in the monkey receiving these high-fat diets some proliferative lesions can reach this range of thickness before undergoing necrosis. Atheromatous aortic lesions characterized by necrosis and the accumulation of lipid debris were found only in monkeys receiving high-fat diets for 70 weeks. In monkeys receiving a diet in which the lipid component was 30% peanut oil and 5% cholesterol, the fatty acid composition of the aorta was similar tothat in humans developing coronary artery atherosclerosis, in that the fatty acids showing the greatest accumulation were oleic and linoleic. The largest number of atheromatous lesions, however, was associated with a diet otherwise identical to the peanut oil-cholesterol diet but containing as its lipid component 30% butter and 5% cholesterol. This latter diet also resulted in higher serum lipid levels and higher aortic lipid levels per milligram of DNA than did peanut oil diet. High-fat diets fed to rhesus monkeys appear to produce both proliferative and atheromatous aortic lesions similar to those seen in the human as regards both light microscopy features and lipid composition. Work is now in progress assessing some of the metabolic features of these lesions.