To determine whether blood pressure modulation account for some/all of the potent suppressive effect of ARB therapy on AAA development, we performed separate experiments in which Ang II/ApoE−/−mice were fed either with the chow supplemented with bosentan, a competitive endothelin-1 receptor antagonist and potent antihypertensive drug with no known influence on AT1a, or with standard chow as its own control. This evidence concerns the gene AGT and triple-A syndrome.