To further delineate the role of CD8+ T cells in AAA pathogenesis, we employed Clec9a−/− mice, which are deficient in cDC1–CD8+ T cell communication.[19] Remarkably, these mice exhibited a reduction in aneurysm expansion similar to that observed in Irf8ΔDC mice (Figure 4I,J). This evidence concerns the gene CD8A and triple-A syndrome.