Cross-dataset comparison showed conserved identities: EC1 (corresponding to our c12 cluster, Cd36+ lipid-handling ECs), EC2 (c11, Fn1+ mesenchymal-like ECs), EC3 (c17, Mmrn1+ lymphatic-like ECs), and EC4 (c13, Lrg1+ pleiotropically activated ECs), underscoring the biological relevance of these EC subpopulations in AAA pathogenesis. This evidence concerns the gene CD36 and triple-A syndrome.