To further prioritize putative causal variants at signals 2 and 3, we aligned the 47 credible variants at these signals with markers of open chromatin (DNase I), active transcription (P300), active enhancers (H3K27Ac, H3K4me1), and breast-relevant TFs (FOXA1, GATA3, ERα) generated in T-47D and MCF-7 breast cancer cells15, 16, 17 (Table S4). This evidence concerns the gene ESR1 and medical procedure.