The JIA animal model revealed that in addition to high levels of expression, HMGB1 also exhibits nucleocytoplasmic translocation and extracellular release as the disease progresses,143 and analysis of human‐derived synovial fluid HMGB1 proved that active release of HMGB1 included acetylation‐dependent/independent mechanisms and various redox modifications, suggesting that HMGB1 plays an important role in the induction and maintenance of inflammatory events in the destructive process of chronic arthritis.144. Here, HMGB1 is linked to juvenile idiopathic arthritis.