To determine which cell types were key to the synthesis and release of CNP in TAA and AAA, we first utilized a mouse strain with endothelium-restricted deletion of CNP13 (crossed to an ApoE−/− background) because this is the major cellular source of CNP in the vasculature.13,18 Ang II–induced aortic expansion was enhanced in the ascending thoracic aorta of ecCNP−/−/ApoE−/−, independent of blood pressure (Figure 3A and 3B; Table 3). The gene discussed is APOE; the disease is triple-A syndrome.