The majority of current RA treatments target either these inflammatory mediators or their critical signalling pathways, e.g. TNF (soluble receptor or blocking antibodies), IL‐6R (blocking antibody), Janus kinases (small molecule inhibitors) or target adaptive immunity, e.g. B cells (anti‐CD20 antibody) or block the interaction between antigen‐presenting cells and T cells [cytotoxic T lymphocyte antigen‐4 (CTLA‐4)]. Here, CTLA4 is linked to rheumatoid arthritis.