Similar to spontaneous atherosclerosis, collar-induced carotid artery plaques in FII−/+:ApoE−/− mice presented a stable pro-fibrotic phenotype, whereas TMPro/Pro:ApoE−/− lesions showed pronounced features of plaque vulnerability, including larger necrotic cores (Figure 2A,D), thin fibrous caps (Figure 2A,E) and significant decrease in collagen content (Figure 3A,B). The gene discussed is APOE; the disease is atherosclerosis.