Atherosclerosis is a multifactorial and long-lasting process in humans. Therefore, animal models where more rapid changes occur can be useful for the study of this process. Among such models are the apolipoprotein (apo) E knock out mice. Apo E deficient mice show impaired clearing of plasma lipoproteins and they develop atherosclerosis in a short time. The current review considers lipid metabolism and inflammation as well as nutritional and pharmacological agents affecting atherosclerosis, using the apo E knock out mouse model.