Similarly, RA pretreatment increased the anti-apoptotic protein B-cell lymphoma-2 (BCL-2) but decreased pro-apoptotic BCL2-Associated X (BAX) and, thus, inhibited the activity of active caspase 3, which were all blocked by wortmannin treatment (Figures 4E,F). This evidence concerns the gene BCL2 and rheumatoid arthritis.