Intriguingly, distinct spatial tissue distributions in pancreatic cancer between different reported CAF populations expressing specific markers may result from different dialogues with tumor cells; inflammatory IL-6+ CAFs, distant from tumor cells, receive an IL-1 signal which triggers the JAK–STAT pathway activation and promotes a CAF inflammatory state, whereas CAFs residing in the vicinity of tumor glands mainly receive a TGFβ signal that favors a myofibroblastic SMA+ state by antagonizing the IL-1 signal [216,217]. This evidence concerns the gene IL1A and pancreatic neoplasm.