CXCL10 (also known as interferon-γ-inducible 10-kD protein [IP-10]) is a chemokine that may play a role in the immunopathogenesis of RA.[13] CXCR3, preferentially expressed on Th1 cells, is the receptor of CXCL10, suggesting that CXCL10 induces the migration of Th1 cells.[13,14] Therefore, we believed that the Th1 cells as well as the activation of Th17 cells contributed to active synovitis in the present case. This evidence concerns the gene CXCR3 and synovitis.