Thus, the adenoviral expression of a multiple mutant apoE4 carrying the L261A, W264A, F265A, L268A, and V269A substitutions in apoE-deficient mice was able to correct the abnormal plasma cholesterol levels without causing hypertriglyceridemia, while a mutant apoE4 bearing the W276A, L279A, V280A, and V283A substitutions failed to correct hypercholesterolemia and caused mild hypertriglyceridemia [52]. Here, APOE is linked to familial hypercholesterolemia.