Interestingly, we uncovered an important function of this subtype in regulating ferroptosis, a form of cell death triggered by iron‐dependent phospholipid peroxidation, which presents a potential therapeutic opportunity to impede cancer progression.[51, 52] It has been reported that CAFs support glutathione synthesis in PDAC through augmenting extracellular cysteine supply, thereby preventing against ferroptosis.[53] In our study, CDCP1+FTL+ CAFs were distinguished by their enhanced iron metabolism and resistance to ferroptosis. This evidence concerns the gene CDCP1 and cancer.