Specific anosmia, the inability to detect a particular odour, has been well documented for decades in human and animal populations. Indeed, the existence of specific anosmias was a favoured argument used to support a receptor‐mediated mechanism of odourant detection prior to the molecular identification of a large family of olfactory G‐protein‐coupled receptors (GPCRs) in the early 1990s (Amoore, 1974; Buck & Axel, 1991). One well known anosmia in humans is the inability to sense 5‐α‐androst‐16‐en‐3‐one (androstenone). Androstenone is variously described as having an unpleasant (urine, sweat) or pleasant odour (sweet, floral), yet a fraction of the population cannot detect its presence. Moreover, androstenone is a pheromone in boars and is found in urine and axillary sweat in humans, making it a prospective candidate for odour‐mediated communication in humans. While a role for androstenone as a human pheromone is open to debate, a widely accepted finding is the ability of humans who are initially insensitive to androstenone to acquire sensitivity to it upon continued exposure (Wysocki et al. 1989). Since the 1989 anecdotal discovery of C.J. Wysocki, several other studies have shown that humans and other species can acquire sensitivity to androstenone as well as to other odourants (Wang et al. 1993; Pause et al. 1999; Dalton et al. 2002). However, the mechanism(s) of this increased sensitivity are poorly understood. In this issue of The Journal of Physiology Wang et al. (2004) provide evidence for a mechanism of increased sensitivity in the olfactory epithelium of humans.