For many complex traits and diseases, numerous associated single nucleotide polymorphisms (SNPs) have been identified through genome-wide association studies (GWAS)through genome-wide association studies (GWAS) [1]. For many of these identified variants it is still unclear through which mechanism the association between the SNP and the trait or disease phenotype is mediated. A complicating factor is that disease-associated variants might not be the real causal variants, but are in linkage disequilibrium (LD) with the true disease-causing variant, making it difficult to accurately implicate the correct gene for a locus in disease pathogenesis.
