Moreover, dasatinib effectively prevented the TGF-β1-induced upregulation of several stem cell-associated genes, some of which are either members of the TGF-β superfamily of ligands (βA activin, BMP2) or function as a co-receptor for TGF-β (CD105/endoglin) and strongly decreased the number of colony-forming units derived from long-term TGF-β1-treated cells assumed to derive from cancer stem cells. This evidence concerns the gene ENG and cancer.