HMGB1 and rheumatoid arthritis: Previous studies have demonstrated that proinflammatory cytokines such as IL-1β or TNFα, as well as LPS and oxidative stress, which are also involved in the pathogenesis of RA, stimulate HMGB1 translocation into the cytoplasm and release in different cell types, such as macrophages, dendritic cells, synoviocytes, and chondrocytes in arthritic joints [32–34].