Future work should therefore prioritize in vivo validation of TTNPB in CAF‐rich pancreatic cancer models, such as co‐implantation of PHLDA1‐high CAFs with orthotopic tumor cells, to assess whether pharmacologic RAR activation can reduce tumor stiffness, limit desmoplasia, and enhance anti‐tumor immunity. The gene discussed is PHLDA1; the disease is familial pancreatic carcinoma.