It is reported that FLS in RA patients are resistant to apoptosis due to the unbalance of the anti- and pro-apoptotic molecules, and the increasing evidences have revealed that anti-apoptotic mediators, such as Bcl-2, Mcl-2, and FLICE-inhibitory protein (FLIP), are up-regulated in the FLS of RA patients whereas the pro-apoptotic proteins, such as tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), p53 up-regulated modulator of apoptosis (PUMA) and Bid, are down-regulated in the FLS of RA patients [29,30,31,32]. This evidence concerns the gene BID and rheumatoid arthritis.