Prior in vitro evidence has suggested that E2 could abate TGFβ signaling in breast cancer cells, and evidence of reciprocal expression of ERα and TGFβR in aggressive breast cancer cells has also been reported [34,35,37,38,39,40], suggesting that the emergence of TGFβ-targeted therapies for advanced stage cancers [21,33] could prove ineffective or less effective for patients with ER+ BMETs, which comprise the majority of breast cancer BMETs. Here, ESR1 is linked to breast carcinoma.