Enhancers rather transcription factors bindingZuber et al. BMC Genomics (2017) 18:Page 9 ofreaders. This is also the first time that such epigenetic readers have been evaluated as enrichment factors for SNPs without prior filtering based on published p-values for risk association. We highlight the possibility that SNPs lying within superenhancers marked by BRD4 are more likely to be associated with an increased susceptibility to BC, PC, and schizophrenia. The expression of the genes regulated by enhancers identified in these diseases could be altered by the presence of specific SNPs lying therein (Additional file 22: Figure S11). This is a concept that has recently been postulated for cancer mutations occurring in a chromatin-specific context [40].Abbreviations AR: Androgen receptor; ARBSs: AR binding sites; BC: Breast cancer; BCAC: Breast Cancer Association Consortium; BRD4: bromodomain containing protein 4; ENCODE: Encyclopedia of DNA Elements; ER: Estrogen receptor; GWAS: Genome-wide association studies; H3K27Ac: Acetylation on Histone 3 lysine 27; iCOGS: Illumina array Collaborative Oncological Gene-environment Study; MED1/MED12: Mediator complex subunit 1/12; PC: Prostate cancer; PRACTICAL: Prostate Cancer Association Group to Investigate Cancer Associated Alterations in the Genome; SNPs: Single nucleotide polymorphisms FPS-ZM1 web Acknowledgements We thank the COGS, PRACTICAL, TRICL and BCAC consortia for access to GWAS summary statistics data. Further details are provided below. The PRACTICAL Consortium (http://practical.ccge.medschl.cam.ac.uk/): Rosalind Eeles1,2, Doug Easton3, Zsofia Kote-Jarai1, Ali Amin Al Olama3, Sara Benlloch3, Kenneth Muir4, Graham G. Giles5,6, Fredrik Wiklund7, Henrik Gronberg7, Christopher A. Haiman8, Johanna Schleutker9,10, Maren Weischer11, Ruth C. Travis12, David Neal13, Paul Pharoah14, Kay-Tee Khaw15, Janet L. Stanford16,17, William J. Blot18, Stephen Thibodeau19, Christiane Maier20,21, Adam S. Kibel22,23, Cezary Cybulski24, Lisa Cannon-Albright25, Hermann Brenner26,27, Jong Park28, Radka Kaneva29, Jyotsna Batra30, Manuel R. Teixeira 31, Hardev Pandha32 1 The Institute of Cancer Research, London, SM2 5NG, UK, 2Royal Marsden NHS Foundation Trust, London, SW3 6JJ, UK, 3Centre for Cancer Genetic Epidemiology, Department of Public Health and Primary Care, University of Cambridge, Strangeways Research Laboratory, Worts Causeway, Cambridge, UK, 4University of Warwick, Coventry, PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/25679764 UK, 5Cancer Epidemiology Centre, Cancer Council Victoria, 615 St Kilda Road, Melbourne Victoria, Australia, 6 Centre for Epidemiology and Biostatistics, Melbourne School of Population and Global Health, The University of Melbourne, Victoria, Australia, 7 Department of Medical Epidemiology and Biostatistics, Karolinska Institute, Stockholm, Sweden, 8Department of Preventive Medicine, Keck School of Medicine, University of Southern California/Norris Comprehensive Cancer Center, Los Angeles, California, USA, 9Department of Medical Biochemistry and Genetics, Institute of Biomedicine, Kiinamyllynkatu 10, FI-20014 University of Turku; and Tyks Microbiology and Genetics, Department of Medical Genetics, Turku University Hospital, 10BioMediTech, 30014 University of Tampere, Tampere, Finland, 11Department of Clinical Biochemistry, Herlev Hospital, Copenhagen University Hospital, Herlev Ringvej 75, DK-2730 Herlev, Denmark, 12Cancer Epidemiology Unit, Nuffield Department of Clinical Medicine, University of Oxford, Oxford, UK, 13Surgical Oncology (UroOncolo.