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ne oThe mouse has become the de facto model for the majority of atherosclerosis studies. Studies involving the quantiWcation of lesions in mouse models of the disease represent the basis of our evolving concepts on the biochemical and cellular mechanisms underlying the atherogenic process. Many issues of experimental design, including speciWc model, strain, gender, atherogenic stimu-lus, duration of study, group size, and statistical analysis may inXuence the outcome and interpretation of atherosclerosis studies. The selection of vascular bed in which to quantify atherosclerotic lesion size could also impact the interpretation of results. Early studies quantiWed atherosclerotic lesion size in either speciWc regions or all of the aortic sinus. Measurement of atherosclerosis throughout the aortic intimal surface has become a common mode for deWning lesion size. It is likely that other vascular regions will be increasingly used. In addition to size, there is an increased emphasis on identifying and quantifying the cellular and chemical com-position of atherosclerotic lesions