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). This evidence concerns the gene IL1B and rheumatoid arthritis.