Possible mechanisms for an increased risk of lymphoma in RA patients include the fact that RA results in persistent immunologic stimulation (which may lead to clonal selection and predispose CD5+ B cells to malignant transformation), decreases the number and function of T-suppressor lymphocytes (including those directed against the pro-oncogenic Epstein-Barr virus), and decreases natural killer cell activity in the synovial fluid, tissue, blood, and lymph [24]. This evidence concerns the gene CD5 and rheumatoid arthritis.