Since we found that the combined stimulation with TGF-β and TNF-α caused hyper-dimethylation at the histone H3K36 residue in breast cancer cells, we further addressed its mechanistic role in regulating the transcriptional activation of MMP-9, following cell stimulations with TGF-β, TNF-α, or TGF-β/TNF-α together. The gene discussed is TGFB1; the disease is breast cancer.