Editorial

The response to anti-TNF-a treatment: gene regulation at the bedside Approximately 40 % of the patients with rheumatoid arthritis do not fulfil the ACR20 response criteria 3 months after initiation of any of the current therapies targeting tumour necrosis factor (TNF-) [1–3]. These patients are not only exposed to an expensive treatment strategy but they also risk serious side-effects, notably the increased risk of tuberculosis. It would clearly be useful if we could identify those patients who are not likely to respond satisfactorily to these therapies or who are likely to develop side-effects. Scientific progress in recent years has offered the promise that indeed such drug effects might be predicted. The elucidation of the complete human genome sequence, the efforts to describe genetic variation in large databases and the introduction of high