In case of tumours that exhibit acquired resistance have developed more heterogeneity and may respond poorly to anti-oestrogens, (2) re-expression of ERα in those tumours with the application of HDAC, DNMT or MEK inhibitors may develop resistance to these inhibitors, (3) since ER-positive breast cancer cells die without ERα and ER-negative breast cancer copes without the receptor, why does one want to give another selective advantage to these tumour cells? Here, ESR1 is linked to neoplasm.