CONCLUSION: The possible association of the C3 gene, inflammatory response, and vascular wall cell biological function alteration with TAAD, despite their unconfirmed role in TAAD. (Anal Quant Cytopathol Histpathol 2021;43:893–900)OBJECTIVE: Stanford type A aortic dissection (TAAD) refers to an acute aortic syndrome that seriously affects human health and even causes death. Little is known about the pathogenesis of TAAD and the factors that determine its development. STUDY DESIGN: In search of differential expression genes (DEGs) in TAAD, the Gene Expression Omnibus database was adopted for the downloading of dataset GSE153434. The generation of DEGs on R software was completed, KEGG pathway analysis and Gene Ontology (GO) enrichment analysis of which were conducted with the R package clusterProfiler. STRING database was used to support the establishment and visualization of the protein-protein interaction (PPI) network. The involvement of DEGs in cell death and growth was revealed by the GO enrichment analysis. RESULTS: The KEGG pathway enrichment analysis identified degeneration of vascular smooth muscle and inflammation as major pathways. The association of the highest-degree complement C3 (C3) in the PPI network with TAAD provides a direction for future research and treatment. © Science Printers and Publishers, Inc.