Abstract These studies consider whether a mild aortic injury that does not increase cholesteryl ester influx during the first few days promotes atheromatosis in the hypercholesterolemic rabbit. The cholesteryl ester influx in uninjured, deendothelialized, and reendothelialized aorta was also measured in order to account for the different cholesteryl ester contents in these areas. By 32–33 days after localized aortic injury which was made after 5–7 days of cholesterol feeding, uninjured (control) areas of the thoracic aortas had accumulated 48 μg/cm 2 each of esterified and nonesterified cholesterol due to continued cholesterol feeding. However, the previously injured deendothelialized and'reendothelialized areas of the aortas had accumulated 6 and 10 times as much esterified cholesterol, and 2 and 5 times as much nonesterified cholesterol, respectively, as the adjacent uninjured areas. Esterified cholesterol influx was low during the second day after injury but increased with time so that 30–31 days later the esterified cholesterol influx in deendothelialized and reendothelialized aorta was respectively 44 and 7 times as great as the 0.1 μg/h/cm 2 in the adjacent uninjured aorta. However, expressed per mg aortic cholesteryl ester, cholesteryl ester influx in reendothelialized aorta was no greater than in noninjured aorta. These studies suggest that an injury that does not initially increase cholesteryl ester influx can promote atheromatosis and that the higher rate of cholesteryl ester influx that develops with time in reendothelialized areas is closely related to its increased cholesteryl ester content.