SMAD4 Endows TGF-β1-Induced Highly Invasive Tumor Cells with Ferroptosis Vulnerability in Pancreatic Cancer

The authors showed that SMAD4 status almost determined the orientation of transforming growth factor β1 (TGF-β1)-induced epithelial-mesenchymal transition via the SMAD4-dependent canonical pathway in PDAC, which altered ferroptosis vulnerability.