RANKL did not alter the level of Bcl-2 in rabbit osteoclasts but caused a marked increase in the level of Mcl-1, an anti-apoptotic member of the Bcl-2 family that is expressed in cells of the myeloid lineage such as macrophages and neutrophils [34,35], and is also known to be increased in synovial macrophages and fibroblasts in RA [36,37] as well as in synovial fluid lymphocytes in juvenile idiopathic arthritis [38]. This evidence concerns the gene BCL2 and rheumatoid arthritis.