Mice are resistant to atherosclerosis and this may be partially due to higher HDL and lower LDL cholesterol levels.75 Although coronary plaque rupture has been difficult to model in mice,75 we confirmed APOL1 accumulation in atherosclerotic lesions, similar to that seen in humans.21 Further, none of the mice in the current study developed kidney disease, as assessed by normal urine albumin excretion and lack of renal pathology. This evidence concerns the gene APOL1 and kidney disorder.