Although the molecular and cellular mechanisms of RA pathogenesis are still controversial, it is now generally accepted that CD4+ T helper (Th) cells play a crucial role in disease manifestation of RA as indicated by abundant infiltration of Th cells in RA joints, human leukocyte antigen (HLA)-DRB1 identified as the strongest disease risk gene for RA, and high efficacy of CTLA4-Ig treatment in RA patients (1–3). The gene discussed is CD4; the disease is rheumatoid arthritis.