Although an increasing number of studies suggest that ferroptosis is involved in the development of rheumatoid arthritis, the specific mechanisms by which this phenomenon occurs remain elusive. The aim of this study was to investigate the genes associated with ferroptosis in RA and their mechanisms of action. We downloaded four gene expression profiles from the Gene Expression Omnibus (GEO) database. After identifying differentially expressed genes (DEGs) between rheumatoid arthritis (RA) synovial tissues and control synovial tissues, basic bioinformatics analyses were performed, including functional annotation, protein-protein interaction (PPI) network, hub gene screening, pharmacogenetic prediction and TF-mRNA-miRNA regulatory network construction. In addition, we analyzed RA immune infiltration according to the CIBERSORT algorithm to assess the relevance of infiltrating immune cells in RA patients. Finally, we identified four hub genes, including CDKN1A, epidermal growth factor receptor, ATF3, and JUN genes, and a total of 92 miRNAs and 14 transcription factors were predicted to form a regulatory network with the hub genes, and 8 drug candidates were screened. These findings may help us to better understand RA pathophysiological changes in basic research, as well as provide new evidence for clinical transformation. We believe that the drug candidates obtained in this study might be helpful for effective therapeutic in RA.