Proposed underlying mechanisms include the enhanced expression of antiapoptotic molecules, such as FLIP and Mcl-1 in RA synovial tissue (169, 170), the reduced expression of the proapoptotic Bcl-2 homology 3 (BH3)-only protein Bim (171), the increased production of TNFα and IL-1 which have antiapoptotic effects (172), and the increased presence of Tregs in the RA joint (173), which do not exert apoptotic effects on monocytes (39). The gene discussed is MCL1; the disease is rheumatoid arthritis.