This is in contrast to the situation in RA, in which IL-1 is strongly TNF-dependent in cultures of synovial cells [32]; these results would indicate that in OA, there is a redundancy between IL-1 and TNF, rather than a 'cytokine cascade' with either of these cytokines controlling the production of the other (Figure 4a). This evidence concerns the gene TNF and rheumatoid arthritis.