Based on these findings, we designated these subpopulations as Cd36+ lipid-handling ECs (c12), Fn1+ mesenchymal-like ECs (c11), Lrg1+ activated ECs (c13), and Mmrn1+ lymphatic ECs (c17), each contributing uniquely to AAA pathogenesis through their distinct molecular and functional characteristics. The gene discussed is FN1; the disease is triple-A syndrome.