The relevance of our findings is that they allow for three inferences. First, they contribute to the debate on the possible synthetic origin of GWAS associations [7], [8], [10], since trans-continental replicability confirms that most –even if not all– of the associations detected by GWAS are not caused by population-specific, rare variants. Second, they clarify the contribution of common variants to extant GWAS results, since practically all GWAS have delivered precisely what they were designed to detect: associations with common variants [1]. Third, our results show that a substantial proportion of causal variants are shared across European and East Asian populations and that they probably lie in the regions close to marker SNPs, which may allow leveraging on the increasingly varied ancestries of GWAS to track them down [25], [36]–[38]. Finally, since larger GWAS did not detect variants with lower frequencies, our findings support a model of common variants of varying effect sizes, closer to the infinitesimal model than to a pure rare variant model of the genetic architecture of disease [4]. However, it is not simple to extrapolate our
