Macrophage infiltration in response to Ang II is crucial in AAA formation and progression in Ang II mouse model of AA.4 Global or cell-specific deletion of CNP in both the endothelial cells and fibroblasts increased proinflammatory (Vcam1, Ccl2, IL-6, Adgre1, NOS2, and IL1β) and anti-inflammatory (Arg1, Slamf1, Mrc1, and IL-10) markers in the aneurysmal abdominal aortas; global deletion of NPR-C−/− also showed a similar pattern of abundance (Figure 8A). This evidence concerns the gene IL1B and triple-A syndrome.