However, this limitation would not affect our main results and conclusions, because (i) ER+ cases constitute the majority (about 80%) of breast cancer and (ii) although binding sites of TFs may slightly vary between ER+ and ER− subtype, we found that the association of breast cancer risk with genetic variations of TF-bindings remained significant for most of our reported TFs (77%) even after we used the aggressive pruning strategy to remove all of the enriched variants which were significantly associated with breast cancer risk (i.e., deflated genome; Supplementary Table 1). The gene discussed is ESR1; the disease is breast carcinoma.