This led to the discovery of a mechanism to maintain continuously active estrogen receptor signaling in ER‐positive breast tumors through loss of DNA methylation at enhancers carrying binding sites for the transcription factors (TFs) ER, FOXA1 and GATA3 [16], and loss of methylation at enhancers carrying binding sites of TFs related to proliferation in ER negative tumors [17]. Here, ESR1 is linked to breast neoplasm.