HDAC9 and breast carcinoma: These results suggest that SFN-mediated HDAC activity allows chromatin remodeling for access of various transcription factors to the hTERT promoter; and DNMTs as well as RBP2-mediated demethylation facilitates repressors such as CTCF and MAD1 to bind to the hTERT gene control region, collectively contributing to hTERT repression in these breast cancer cells.