Answering to these questions is pressing for two reasons. First, the description of the genetic architecture of disease lies at the foundation of personalized medicine and, in particular, finding predictors of individual disease risk that could be applicable to different ancestries would be a major step forward [1] and would also allow the development of prioritizing strategies to identify disease-associated loci. Second, if sharing of causal variants across populations were common, it would suggest trans-ethnic mapping as a powered tool that would take profit of population heterogeneity in LD and allele frequencies to identify the causal variants underlying disease susceptibility [1], [15].
