However, in general, most animal models of atherosclerosis do not develop thrombosis due to plaque rupture.122 Triggering thrombus formation, for example, by FeCl3 injury only replicates the final stages of atherothrombotic disease.123 Nevertheless, FeCl3 or needles have been used to induce thrombus formation in atherosclerosis-relevant models (eg, mice deficient in apolipoprotein E).124–126 Analysis of the corresponding thrombi compositions in relevant models for atherosclerosis may provide new insights in thrombus structure in the context of cardiovascular disease. The gene discussed is APOE; the disease is atherosclerosis.