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 results to associations that so far remain undiscovered. Whether the heritability that is not yet explained by GWAS will be partly due to risk variants in insufficient LD with common SNP markers, as suggested by some authors [6], [39] or whether this heritability exists at all [40] will only be resolved by further empirical research.
