Interestingly, CTHRC1+ CAFs exhibit significant functional plasticity across pathological contexts: in pulmonary fibrosis, they enhance tumor aggressiveness via the TGFβ1‐SFRP1 axis [25]; in lung cancer, they promote chemoresistance through TGF‐β/Smad3 signaling and a glycolysis/H3K18la positive feedback loop [34]; in pancreatic cancer, prior studies revealed spatial colocalization of CTHRC1+ CAFs with SPP1+ macrophages within PDAC microenvironments, where they collaboratively drive tumor progression by promoting fibrosis, immunosuppression, and epithelial‐mesenchymal transition [35]. The gene discussed is SPP1; the disease is neoplasm.