However, during RA, synovial fibroblasts (SFs) undergo a pathogenic transformation that destabilizes the normal function of the synovium and triggers inflammatory mechanisms, such as recruitment of immune cells, production of inflammatory cytokines (IL-6, CCL2, MCSF, RANKL), formation of ectopic lymphoid-like structures and responses to inflammatory factors (IL-1β, TNF, IL-17) (4–6). This evidence concerns the gene TNF and rheumatoid arthritis.