Histone deacetylases (HDACs) are negative regulators of ERα transcription, and HDAC inhibitors, including suberoylanilide hydroxamic acid (SAHA, vorinostat) and trichostatin A, have been shown to reactivate ERα expression in ERα−negative breast cancer cells and reverse TAM resistance in preclinical studies.6, 7, 8 Encouragingly, in phase II clinical trials, the combination of vorinostat and TAM showed promising activity in reversing hormone resistance.9 The gene discussed is HDAC9; the disease is breast carcinoma.