Hidradenitis suppurativa (HS) is a severe, chronic inflammatory disease characterized by inflammatory nodules, progressive sinus tracts, and fistulas. Currently, its pathogenesis remain incompletely understood, and while diverse treatments are available, these have suboptimal efficacy. Herein, we analyzed the relevant genes and pathways in HS using bioinformatics to provide directions for the development of novel treatment.Two HS datasets were obtained, and differentially expressed genes associated with HS were identified. Enrichment analysis was performed, and a protein-protein interaction network of differential genes was produced. Genes were analyzed using the CytoHubba plugin to obtain the hub genes. For validation, we analyzed the differentially expressed genes between the affected skin tissues of patients with HS and normal human skin tissues.Overall, 180 differential genes associated with HS were identified. Differentially expressed genes were mainly enriched in leukocyte migration, serine hydrolase activity, and serine-type peptidase activity. In total, 69 transcription factors, 115 microRNAs, and 41 drugs associated with hub genes were identified. The expression of FCGR2A and IL2RG was significantly upregulated in the HS disease group compared with that in the normal group.Ten hub genes were identified. Among these, FCGR2A is responsible for the phagocytosis and clearance of immune complexes, the dysregulation of which may represent an important link in the pathogenesis of HS. The PI3K-Akt-mTOR signaling pathway, regulated by the IL2RG gene, showed a close relationship with HS severity and the mechanism of scarring, presenting a potential drug target. The miR-3689 targeting the gene FCGR2A might also be potential biomarkers.