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. Author manuscript; available in PMC: 2013 Sep 12.
Published in final edited form as: Science. 2012 Sep 5;337(6099):1190–1195. doi: 10.1126/science.1222794

Fig. 4. Common disease networks.

Fig. 4

GWAS SNPs from related diseases repeatedly perturb recognition sequences of common transcription factors. Shown are factors whose recognition sequences harbor ≥8 or ≥6 GWAS SNPs in inflammatory/autoimmune diseases (A) and cancer (B), respectively. Edge thickness represents number of associations between TF and disease in DHSs in relevant tissues. Both networks are significantly enriched for overlap with disease-relevant GWAS SNPs, and include many well-studied regulators.