In order to define the contribution of A20 to rheumatoid arthritis pathology, Matmati and colleagues generated mice lacking A20 in myeloid cells (A20myel‐KO) and determined that such mice develop severe features of rheumatoid arthritis‐like destructive poly‐arthritis, high serum levels of IL‐6, TNF, IL‐1β and MCP‐1 and prolonged NF‐κB activation in macrophages, demonstrating the cell‐specific function of A20 in causing a rheumatoid arthritis‐like pathology 209. This evidence concerns the gene TNF and rheumatoid arthritis.