In thoracic aortas, the effects of TGF-β neutralization have ranged from reducing aneurysms in fibrillin1 haploinsufficient mice [11] and AngII-infused CXCL10 deficient mice [15], while having no effect on aortic disease in mice expressing functionally deficient TGF-β receptors [20] to promoting ascending aortic rupture in fibrillin1 hypomorphic mice [12]. The gene discussed is AGT; the disease is aneurysm.