Moreover, Wnt/β-catenin signaling also has an important role in the regulation of CSC self-renewal and tumorigenesis.41 Excessive Wnt/β-catenin signaling is required to maintain CSC capabilities in colon cancer, glioma and mixed lineage leukemia.22 Importantly, Scheel et al.42 reported TGF-β and Wnt signaling interact to induce activation of the epithelial–mesenchymal transition and maintain a CSC-like state, and inhibition of both the TGF-β and Wnt/β-catenin pathways significantly inhibited the metastatic and self-renewal abilities of primary mammary epithelial cells. This evidence concerns the gene TGFB1 and colonic neoplasm.