Loss- and gain-of-function studies were used to elucidate the possible role of nuclear SDC1 in regulating EMT in two human tumor cell models: (i) human lung A549 adenocarcinoma cells, which are of epithelial origin but have the capacity to undergo EMT after exposure to TGF-β1 [26], and (ii) human B6FS fibrosarcoma cells, which are of mesenchymal origin and have been used in previous studies to identify a role of nuclear SDC1 in regulating cell proliferation [27]. The gene discussed is SDC1; the disease is neoplasm.