IFN‐γ can restrict the Th17 response and exacerbation of arthritis in an animal model of RA was found in IFN‐γ receptor‐ and IFN‐γ‐deficient mice.[48] A defect in the IFN‐γ response has been found in lymphocytes of patients with RA.[49] In the present study, IFN‐γ had dual effects on FLS; IFN‐γ can induce a regulatory phenotype by upregulating the expression of inhibitory molecules and also induce pro‐inflammatory characteristics of FLS by promoting IL‐6 production. Here, IFNG is linked to arthritic joint disease.