The co-treatment with inhibitors of DNA methyltransferase-1 (DNMT-1, such as 5-aza-2-deoxycytidine (AZA)) and histone deacetylase (HDAC, such as Trichostatin A (TSA) and suberoylanilide hydroxamic acid (SAHA)) induce ER gene expression in ER(−) breast cancer cells and restore sensitivity to antiestrogen [59,63–66]. Here, ESR1 is linked to breast carcinoma.