TGF-β1 plays an important role in cancer migration due to its medication towards CAF contractility and MMP secretion, where CAFs produces MMPs to lose the structure of TME architecture via both canonical and non-canonical TGF-β signaling pathways, i.e., non-canonical pathways cause RhoA/ROCK to promote MyoII contractility, while canonical pathways enhance SNAIL1 and TWIST1 gene transcription for increasing CAF contractility [84,88]. Here, TWIST1 is linked to cancer.