CCL5 was directly trans-activated by cancer-Foxp3, which in turn promoted Treg infiltration.24 Intriguingly, Jang et al. reported accumulation of Tregs around murine pancreatic tumours within one week of implantation, suggesting tumour cell-intrinsic secretion of CCL5 plays an important role in this rapid infiltration.25 This proposes a model of cell intrinsic CCL5 secretion resulting in autocrine and paracrine signalling promoting a pro-tumourigenic immunosuppressive TME. Here, FOXP3 is linked to pancreatic neoplasm.