There has been speculation that an atopic predisposition might increase susceptibility to cancer, although convincing evidence has been lacking. An exception is prostate cancer, for which a positive association with atopy1, and especially dust mite sensitisation2, has been reported, but not explained. A strong predictor of prostate cancer risk is raised levels of IGF-13. The observation that Th2 cytokines promote the expression of IGF-14 is in keeping with the hypothesis that atopy may increase risk of prostate cancer. However, it is also possible that IGF-1 may drive atopy. Laboratory studies have suggested that IGF-1 promotes Th2 responses and raised IgE5;6. Furthermore, IGF-1 is a primary mediator of the effects of growth hormone, and cord blood IGF-1 levels are positively associated with size at birth7. This may have relevance to the, albeit inconsistent, evidence linking enhanced fetal growth with atopy8;9. Interestingly, IGF-1 levels fall with increasing parity10, raising the possibility that IGF-1 might partly explain the relation between parity (birth order) and atopy in the offspring. However, epidemiological studies on the relation between IGF-1 and atopy are lacking.