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. This evidence concerns the gene SFN and breast cancer.