An AAA induces the upregulation of proinflammatory genes, such as protein tyrosine phosphatase receptor type C (PTPRC), C-X-C motif chemokine ligand 8 (CXCL8), lymphocyte-specific protein tyrosine kinase (LCK), C-C motif chemokine ligand 5 (CCL5), and MMP-9, while suppressing the expression of the anti-inflammatory gene peroxisome proliferator-activated receptor gamma (PPARγ), thereby contributing to inflammation in the adjacent aortic wall and playing a role in the pathophysiology of AAA (Meekel et al., 2021). This evidence concerns the gene CXCL8 and triple-A syndrome.