The IF analysis revealed upregulated levels of H3K18la and increased CD86 expression in the AAA group, and H3K18la co-localized with CD86 in the aortic aneurysm, suggesting both an expansion of M1 macrophages and enhanced H3K18la levels within these M1 macrophages during AAA pathogenesis (Fig. 1H). This evidence concerns the gene CD86 and triple-A syndrome.