Enhancers may lie at great distances from the gene(s) they control (17) and function through long-range regulatory interactions (4, 18), complicating the identification of target genes of regulatory GWAS variants. Most DHSs display quantitative, cell-selective DNase I hypersensitivity patterns which may be systematically correlated with DNase I sensitivity patterns at cis-linked promoters. DHSs that are strongly correlated (r > 0.7) with specific promoters function as enhancers that physically interact with their target promoter as detected by chromosome conformation capture methods including 5C and ChlA-PET (10).
