Extensive investigations of the pathogenetic mechanisms of inflammation and autoimmunity and the resulting increased understanding of cytokine networks and cellular players in rheumatoid arthritis (RA) have led to the development of agents that block tumour necrosis factor (TNF)α, interleukin (IL)-1 and IL-6 signalling, or target pathogenic cells such as B cells and osteoclasts [1,2]. Here, TNF is linked to rheumatoid arthritis.