Knocking out Olfr168 increased both the rate of aortic growth and the incidence of aortic rupture in a mouse model of AAA, while treatment with the terpene (−)-carvone, an exogenous agonist of OR2L13, attenuated AAA growth in a manner that paralleled that of aspirin-based therapies [82]. The gene discussed is OR2L13; the disease is triple-A syndrome.