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I read with interest the recent article by Crilly and colleagues1 on the potential use of interleukin 1 (IL1) gene polymorphisms in predicting the need for joint surgery in patients with rheumatoid arthritis. Although the authors' findings are certainly interesting and worthy of further investigation, I would like to raise a couple of points as to how these were arrived at in the first place.
When adopting the “candidate gene” approach in any disease association study, it pays to consider carefully the physiological context of a hypothesis. In this case the authors worked on the premise that one of the IL1 gene family polymorphisms investigated might correlate with disease outcome. These included polymorphisms both in the IL1 genes and the IL1 receptor …