Given that ARID1A binds within ER-bound enhancers and thereby regulates ER-dependent transcription, it has been suggested that the wild-type ARID1A expression is related to a better clinical outcome in ER+ breast cancer patients, where fulvestrant combined with ARID1A inhibitor could be promisingly used for ER+ breast cancer, whereas ARID1A inactivating mutations are enriched in treatment-resistant tumors and metastases (in total 12% of cases) and ARID1A inactivation is thereby considered to be a tumor-promoting event in ER+ breast cancer (69–72). The gene discussed is ESR1; the disease is breast carcinoma.