In the context of observational studies, it is reasonable to assume that revealing a ‘true’ Se-cancer risk association may only be possible, when the range of Se statuses in the study sample encompasses both deficient or suboptimal, as well as optimal concentrations of selenoproteins relevant to a particular type of cancer [44].This may have been the case in the recently published case–control study nested in the whole EPIC cohort on Se status and CRC risk [45]. The gene discussed is SELENOS; the disease is cancer.