In summary, these data suggest that innate immune cells, in particular monocytes/macrophages, rather than stromal cells account for the beneficial effects of Has3 deficiency in our model of AAA: Due to reduced HAS3-mediated HA-CD44 immune cell infiltration and the subsequent attenuated degradation of the aortic wall, there is ultimately less destabilization and rupture of the vessel wall (Figure 6). The gene discussed is HAS3; the disease is triple-A syndrome.