identify functional regulatory variants [82]. However, hundreds of candidate SNPs may remain even after prioritization, especially when the locus harbors an enhancer cluster. This was illustrated in a recent survey of breast cancer risk loci, which showed that 921 SNPs co-localize with putative enhancers in human mammary epithelial cells across 71 risk loci [8]. Similarly, 663 enhancer SNPs were identified for 77 prostate risk loci [6]. Furthermore, while some enhancer variants influence transcription factor binding [6,28,29,34], SNPs do not necessarily have to reside within a TFBS to influence transcription factor binding or enhancer activity [33,73,74,83]. It is clear that massively parallel reporter assays (discussed above) will be necessary to help distinguish functional variants from those that are passengers.
