Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by joint and systemic inflammation.[1, 2, 3] The dysfunction of regulatory T cells (Tregs) plays a crucial role in the breakdown of self‐tolerance,[4, 5] leading to a proliferative autoimmune disorder within the peripheral blood and the infiltration of inflammatory immune cells (including proinflammatory M1 macrophages[6, 7] and pathogenic CD4+ T cells[8, 9]) into the synovial membrane. Here, CD4 is linked to rheumatoid arthritis.