It has been shown that inflammation in RA is mediated also through recruitment of lymphocytes to the site of inflammation [47] and our group could previously demonstrate that TNF-β treatment of chondrocytes with increased dosages of TNF-β resulted in an almost 2fold increase in the adherence of T-lymphocytes [14], highlighting a novel role for TNF-β in supporting an inflammatory milieu and stimulating ongoing inflammation in chondrocytes. The gene discussed is LTA; the disease is rheumatoid arthritis.