Studies made in transgenic mice have shown that apoE-deficient animals, which develop hypercholesterolemia and are prone to spontaneous atherosclerosis, show decreased lesion size when overexpressing human apoAI [21], suggesting that apoE and apoAI operate together to optimize mobilization of macrophage cholesterol, a process critical to limiting plaque development. This evidence concerns the gene APOE and familial hypercholesterolemia.