In a recent work, PrPC silencing attenuated the characteristic molecular landscape of a CRC–CSCs subpopulation with mesenchymal phenotype, through the recruitment of the Hippo pathway effectors YAP and TAZ and the TGFβ pathway, suggesting that PrPC deregulation could contribute to a CSCs phenotype in CRC [68]. This evidence concerns the gene TGFB1 and colorectal carcinoma.