In addition, synovial hyperplasia in RA appears to be caused at least in part by the impairment of apoptosis in RA-FLSs and synovial macrophages, while deficient apoptosis has been shown to prolong RA-FLS survival by increasing the production of anti-apoptotic molecules like B-cell lymphoma 2 (Bcl-2), sentrin-1 (SUMO-1), and Fas-associated death domain-like interleukin-1- converting enzyme inhibitory protein (FLIP) [19, 20]. This evidence concerns the gene SUMO1 and rheumatoid arthritis.