Studies conducted in breast cancer demonstrated that the unmodified transcription factor Sp3 induces transcriptional repression of TGFβRII promoter [7]; consequently, treatment with histone deacetylase inhibitor, Trichostatin A (TSA), results in acetylated Sp3 which alleviates transcriptional repression of TGFβRII gene expression [8]. This evidence concerns the gene SP3 and breast carcinoma.