Objective: To explore potential genes associated with the formation and rupture of intracranial aneurysms based on the Gene Expression Omnibus (GEO) database. Methods: A total of 133 mRNA microarrays were collected from the GEO database. Differential mRNA gene analysis was performed on the data of each group in the GEO2R platform, and the common differential genes were screened and the gene ontology enrichment analysis and the Kyoto Gene and Genomic Encyclopedia pathway enrichment analysis were completed. The screened differential genes were introduced into the String online database to obtain the interaction between the proteins encoded by the differential genes. Results: Forty-two common differential genes were screened, and the main biological processes involved included the transcriptional regulation of oxidative stress, the positive regulation of chemokine production, and the positive regulation of autophagy of giant cells by RNA polymerase II promoter. Molecular functions included protein binding, RNA polymerase II transcriptional co-repressor activity, transcriptional activator activity, and protein kinase C binding. The main signal pathways covered included hypoxiainducible factor-1 signaling pathway, glucagon signaling pathway, and metabolic pathway signaling pathway. Conclusions: The formation and rupture of the intracranial aneurysm may be initially screened with amidoxime reduction component 1, tumor necrosis factor-α- inducible protein 6, haptoglobin, mast cell membrane-expressing protein 1, zipper containing kinase, phospholipase Cβ4 and blood and nervous system expression factor-1. In addition to the previously knownintracranial aneurysms mechanisms, cellular autophagy and hypoxia inducible factor-1 pathway may also be involved in the formation of intracranial aneurysms.