From the other hand, ERα‐36 signaling has been shown to facilitate the transition of ERα+ breast cancer cells from an epithelial to a mesenchymal state, by activating certain EMT‐associated molecules, including transcription factors such as ZEB1, Snail1, vimentin, and CXCR4, while simultaneously downregulating the expression of E‐cadherin (Fig. 4) [10, 46]. This evidence concerns the gene ESR1 and breast cancer.