The hyperplastic synovium observed in RA may result from the hyperproliferation of FLSs, which in turn stimulate the expression and release of inflammatory cytokines such as TNF-α, IL-1β, IL-6, CXCL8, IL-12, IL-17A, IL-21, IL-22, IL-23, interferon (IFN)-α, and IFN-γ, as well as apoptosis resistance due to defects in tumor protein p53. This evidence concerns the gene IFNG and rheumatoid arthritis.