Nevertheless, the aortic nitrate content of Bdkrb2–/–ApoE–/– mice was not normalized to B6 control level by B2 bradykinin receptor deficiency (Figure 4A), most likely because defective NO generation in atherosclerotic Bdkrb2–/–ApoE–/– mice has additional causes, which are independent of Bdkrb2, e.g., ApoE deficiency-induced hypercholesterolemia. This evidence concerns the gene BDKRB2 and familial hypercholesterolemia.