Hot topics in science, like fashion, come and go. Asthma genetics is no exception to this rule. Asthma candidate genes come and very few stay for good, changing from “candidate” gene to “disease” gene. Only an exclusive few survive a thorough replication process.

The asthma candidate genes studied in the replication approach by Blakey and colleagues1 (pages 381–7) were originally discovered by positional cloning, a technique based on linkage studies using microsatellite markers and subsequent fine mapping of these linkage signal loci in families. Until recently, when genome-wide association studies (GWAS) entered the field, this was the method of choice to detect novel asthma candidate genes. In contrast to candidate gene studies, which are hypothesis driven and always only as good as the underlying hypothesis, positionally cloned genes had the aura of being the better asthma candidate genes, as they were …