Booms A, et al. – In previous genome-wide association studies, more than 142 loci have been shown to govern breast cancer genetic predilection. Thus researchers performed the current study to gain clarity on the functional contribution of these risk loci to breast cancer. By histone H3K27 acetylation and CTCF occupancy, they identified active regulatory elements (enhancers, promoters, and chromatin organizing elements), and ascertained the enrichment of risk variants at these sites. A comparison of these findings with earlier published data and for other cell lines, including human mammary epithelial cells, was performed. Also, these data were associated with gene expression. Findings revealed likely functioning of 10 (of 142) breast cancer risk loci via enhancers that were active in MCF-7 and were well suited to targeted manipulation in this system. In contrast, the inability of mapping of risk loci to specific CTCF-binding sites was revealed, and functional enrichment was not exhibited by the genes linked to risk CTCF sites. As suggested by the identity of risk enhancers and their related genes, some risk may function during later processes in cancer progression.