Histologic evaluation of hematoxylin-eosin-stained aortic specimens from the different groups of ApoE–/– mice confirmed the enhanced atherosclerosis progression of Tg-B2++/ApoE–/– mice by an increased intimal atherosclerotic lesion area in the aortic arch of Tg-B2++ApoE–/– mice with transgenic BDKRB2 expression compared to ApoE–/– mice with endogenous Bdkrb2 expression, and double-deficient B2–/–ApoE–/– mice (Figures 4C,D). The gene discussed is APOE; the disease is atherosclerosis.