TNF and rheumatoid arthritis: SF are essential players in RA pathophysiology, undergoing significant hyperplasia in rheumatoid arthritis (RA) and responding to exogenous proinflammatory stimuli, particularly to TNFα, by producing a large variety of proinflammatory, bone destructive and cartilage-destructive mediators [10] thus contributing to perpetuate the inflammatory milieu in the joint.