Anti-ENO1 antibodies were reported to contribute to the perpetuation of synovial inflammation in RA by stimulating monocytes and macrophages to produce increased amounts of proinflammatory mediators, such as TNF-α, IL-1α/β, IFN-γ, and PGE2 via the p38 mitogen activated protein kinase and NF-kB pathways [48]. The gene discussed is IFNG; the disease is inflammatory response.