The interaction between CD2 and CD58 could promote T cells and macrophages to secrete chemokines and cytokines establishing the inflammatory environment, resulting in the formation of atherosclerotic plaque in psoriasis patients, yet the role of CD2/CD58 in the communal pathogenesis of RA and AS still lacks relevant evidence and needs to be further explored (86). The gene discussed is CD2; the disease is rheumatoid arthritis.