We have shown that in the mouse model of AngII-induced AAA there is a differential response to the aneurysmal effects of AngII as indicated by the variation in the size and time of AAA occurrence, and that the degree of macrophage accrual may be relevant to the observed differential response to AngII, with the extent of hypercholesterolemia as the potential underpinning factor. This evidence concerns the gene AGT and familial hypercholesterolemia.