Although a previous study reported that IL-26 increased the secretion of IL-1β, IL-6, and TNF-α by myeloid cells in RA synovial fluid [8], we did not observe upregulated levels of these cytokines in IL-26-stimulated RA-FLSs, suggesting that IL-26 did not mediate the production of proinflammatory cytokines in RA-FLSs. The gene discussed is IL26; the disease is rheumatoid arthritis.