The aetiology of human RA has not been fully elucidated, but the current hypothesis is that deregulation of interleukin (IL)-17 production is the driving force behind activation of T and B cells as well as macrophages, which release cytokines such as IL-1, IL-6 and tumour necrosis factor (TNF)-α [1]; this is supported by experiments in mice deficient for either IL-17 or IL-23, the latter a cytokine essential for T helper type 17 (Th17) cell survival, as both types of ‘knock-out’ mouse are resistant to the development of collagen-induced arthritis (CIA) [2,3]. The gene discussed is IL17A; the disease is rheumatoid arthritis.