APOE and familial hypercholesterolemia: When SR-BI KO mice are crossed with mice having homozygous null mutations in the apolipoprotein E (apoE) gene, the progeny SR-BI/apoE double knockout (dKO) mice exhibit severe hypercholesterolemia, dramatically enlarged and abnormal HDL particles and numerous cardinal features of human coronary heart disease (CHD) [4], [5].