ESR1 and breast cancer: Furthermore, treatment with AZA/TSA in ERα-negative cell lines increased chromatin accessibility for AP-2γ and polymerase II binding at the ERα promoter, which consequently allows AP-2γ-driven ERα expression in ERα-negative cells, suggesting that AP-2γ is a crucial transcription factor for ERα gene expression in breast cancer cells.[44] AP-2γ might also regulate ERα expression and activity via forming complexes with other proteins.