In both organisms, we uncovered that CXCL12, MFAP5, and EMP1 might participate in the pathogenesis of AAA, among which it had been reported that the blockade of CXCL12/CXCR4 protected against AAA formation (Michineau et al., 2014), whereas several collagen genes (COL1A1, COL1A2, COL3A1, and COL5A2); some reported virulence genes for TAA (LOX, COL3A1, and MMP2)(Longo et al., 2002; Shen et al., 2015; Pinard et al., 2019; Chen et al., 2022); and potential causative genes (CTHRC1, SERPINH1, SPARC, THY1, and CTSK) were identified involving in the pathology of TAAs (Figure 3F). This evidence concerns the gene COL1A2 and triple-A syndrome.