In murine models, inflammation is the primary driver of AAA progression in the first two weeks of AAA expansion [40,41]; thus, this could explain why we, in this study, did not observe any effect of CAG on the monocyte/macrophage marker F4/80 at the mRNA level, along with no reduction of CD68 positive macrophages in the wall of the CAG treated aneurysms. The gene discussed is CD68; the disease is triple-A syndrome.