IL‐6 exacerbates OA progression by inhibiting the synthesis of type II collagen, the main component of the ECM.23 In OA patients, an increased circulating level and over‐expression in synovial fluids of IL‐6 have been described.24 A previous study implicated FSTL1 in the pathogenesis of reactive arthritis, RA and lumbar disc herniation. This evidence concerns the gene IL6 and rheumatoid arthritis.