Myeloid‐derived macrophages accumulate in the RA synovium and differentiate into M1 macrophages, which produce proinflammatory cytokines such as tumor necrosis factor‐alpha (TNF‐α), interleukin (IL)‐6, and IL‐1β, thereby exacerbating synovitis.[10, 11] Crosstalk between FLSs and macrophages may represent a critical mechanism underlying synovitis.[12, 13] Synovial vessels are essential for the expansion of synovial tissue and the development of RA synovitis.[14, 15, 16]. Here, IL1B is linked to rheumatoid arthritis.