In the autoimmune disease rheumatoid arthritis (RA), overexpression of E2F1 has also been shown to suppress the proliferation and invasion of RA fibroblast-like synoviocytes and the production of proinflammatory cytokines via the p53 signaling pathway, and it has been suggested that this may offer new targets for treatment [16]. This evidence concerns the gene TP53 and autoimmune disease.