Fibroblast-like synoviocytes can respond to proinflammatory environments and then themselves become effectors for driving disease pathology, and hence are called “passive responders and imprinted aggressors”.9 In support of their activated phenotype, here we demonstrate that FLS obtained from human OA and RA patients and from cell outgrowth of mouse patella can respond to TNF-α stimulation to increase secretion and expression of several proinflammatory mediators. Here, TNF is linked to rheumatoid arthritis.