The improvement in RA treatment with the new targeted therapies also supports the importance of monocytes in disease activity by either i) blocking monocyte-derived cytokines (TNF, IL-6), ii) suppressing monocyte activation by T cells via CTLA4 (abatacept), or iii) inhibiting Janus kinases in intracellular signaling following cytokine stimulation, particularly by TNF and IL-6 [49]. The gene discussed is CTLA4; the disease is rheumatoid arthritis.