The available reports on the allele frequency distribution of GWAS risk variants point at an excess of common variants [16] that, at least for some particular diseases [17], present consistent effects across populations. If repeated, these observations constitute empirical evidence against rare alleles as a source of synthetic associations and would point at common variants that are in LD with the associated tagSNPs in all populations. However, such studies have not been generalized across different diseases and, currently, most evidence accumulating in the field comes from either re-sequencing efforts aimed to capture rare variants [18] or multi-ethnic replication efforts for a few risk variants [13], [15], [17], [19]. In addition, most meta-analysis of GWAS data, that could shed light on these issues, either have ignored population heterogeneity [2], [20] or have focused on a limited set of traits [21] and GWAS [22].
