TGFB1 and neoplasm: This suggests that SAS-δ can drive aggressive malignancy more strongly than p-SAS, and that SAS-δ can generate invasive tumors in vivo in response to various growth factors, including TGF-β1, in the tumor microenvironment and in response to accidental DNA damage that induces genetic mutations or epigenetic abnormalities that suppress SLUG expression (which ultimately allows stable SLUG-pT208 proteins to concentrate efficiently at their transcriptional target sites on chromatin) in oral cancer cells.