In contrast to the long‐standing notion that E‐cadherin promotes the resistance of 2D tumor cells to ferroptosis (Figure 5),18 deletion of E‐cadherin, a key factor in EMT, does not sensitize 3D CRCs to ferroptosis, but unexpectedly induces a late hybrid EMT state and superdefense against ferroptosis through integrin‐mediated tension and mitochondrial reprogramming. The gene discussed is CDH1; the disease is neoplasm.