Previous experiments have shown that local irradiation of the carotid arteries of hypercholesterolemic rabbits results in the development of atheromatosis in the irradiated areas of the arteries. The process starts with the adherence of monocytes to the endothelial layer, their entrance into the subendothelial space, and their subsequent transformation into lipophages (foam cells). Prevention of this type of plaque formation can be achieved by prednisolone (in a lower concentration than previously used) (Vos et al. 1981) and by VP16-213 (Vepesid). Differential blood cell counts demonstrated that the animals subjected to treatment with prednisolone developed a moderate relative lymphocytopenia, whereas treatment with Vepesid resulted in a severe monocytopenia. Since prednisolone treatment only partially prevented plaque formation, whereas Vepesid seemed to fully inhibit the development of plaques, we conclude that although a role of the lymphocyte in the process of plaque formation cannot be excluded, the monocyte seems to play a crucial role in the pathogenesis of radiation-induced atheromatosis.