In the inflamed joint, the uncontrolled proliferation and accumulation of fibroblast-like synoviocytes (FLS) are the main cause of chronic inflammation and its progression to joint damage3, 4. This results in part from acquired molecular changes in FLS leading to reduced sensitivity to cell death signals. Apoptosis-inducing strategies targeting FLS have been considered as treatment of arthritis5–7. In vitro experiments using a plasmid vector to express the proapoptotic gene PUMA (p53 upregulated modulator of apoptosis) in FLS, showed the efficacy of PUMA in inducing cell apoptosis8, 9, a phenomenon which was independent of the p53 status of the synovium9. These preliminary data suggested that the strategy of PUMA-induced apoptosis in FLS could block the hyperplasia of the synovial intimal lining.