Of note, we have recently demonstrated that bone marrow CD34+ cells from RA patients have abnormal capacities to respond to tumor necrosis factor (TNF)-α and to differentiate into fibroblast-like cells producing MMP-1, suggesting that bone marrow CD34+ progenitor cells might generate type B synoviocytes and thus could play an important role in the pathogenesis of RA [2]. This evidence concerns the gene CD34 and rheumatoid arthritis.