For example, both in hFibromyocyte and mSMC3, we identify potential causative genes for AAA (CXCL12, MFAP5, and EMP1), among which the blockade of CXCL12/CXCR4 protects against AAA formation (Michineau et al., 2014), and distinct pathogenic genes for TAA [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 other unreported genes (CTHRC1, SERPINH1, SPARC, THY1, and CTSK)]. Here, CTSK is linked to triple-A syndrome.