The increase of Bcl-2, Bax and Bcl-xl formed two heterologous dimers, inhibited downstream apoptotic cascade, thereby affecting the activation of apoptotic protease, causing the imbalance between synovial cell proliferation / apoptosis, leading to excessive proliferation of synovial cells, aggravation of RA disease. The gene discussed is BCL2; the disease is rheumatoid arthritis.