The lack of replication may implicate false positive findings. Alternatively, it may be due to lack of power in the replication sample, population specificity of the associations, as well as gene‐environment interactions. In addition, our study sample comes from one of the best‐characterized founder populations, the Finns. Unique LD patterns are observed in founder populations (Service et al. 2006); thus, the lack of replication may at least partly be due to the genetic heterogeneity between the discovery sample (Finns) and replication sample (Australians). It has been shown that population isolates, especially those founded recently, such as Finland, have longer stretches of LD than outbred populations and may thus achieve better genome‐wide coverage with equivalent numbers of markers (Peltonen et al. 2000; Service et al. 2006). Our top SNPs may tag underlying functional variants in the Finnish sample, but due to differences in LD structures the functional variants are not necessarily captured by these SNPs in the Australian data. Population‐specific functional variants are known to exist (Lim et al. 2014), and one has already been documented in the Finnish population for a behavioral trait (Bevilacqua et al. 2010).
