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Modern molecular biology offers a unique opportunity to gain a comprehensive picture of gene expression in a disease state. This review presents recent findings in the field of synovial fibroblast biology contributing to knowledge of the pathogenesis of rheumatoid arthritis.Recently it has become apparent that innate immune response pathways play a critical role in driving synovial activation and contribute significantly to the turnover of leukocytes in the synovial compartment. In addition, microparticles have been identified as a new class of potent mediators, broadening the known spectrum of cell-derived modulators in the joint. Numerous research groups gained new insights into detailed molecular mechanisms leading to the invasiveness of rheumatoid arthritis synovial fibroblasts, the disturbance in the regulation of apoptosis, and synovial cell–cell and cell–matrix interactions.The key role of synovial fibroblasts in the pathogenesis of rheumatoid arthritis has been highlighted by the fact that these cells not only are the main executors of cartilage and bone destruction but also modulate numerous interactions in rheumatoid joints. Moreover, it has become evident that integration of a large body of information is indispensable to get a comprehensive outlook on synovial activation in the pathology of rheumatoid arthritis.