Macroscopic examination of the aortas revealed that only 5% of the WT mice (1 of 20) developed dissecting AAA in response to Ang II administration, whereas Plod1-/- mice exhibited significantly aggravated remodeling of the aorta, with 50% of the mice (10 of 20) developing dissecting AAA formation and 40% of the mice (8 of 20) experiencing rupture events (Figure 1A-B). The gene discussed is AGT; the disease is triple-A syndrome.