In a Pan02 pancreatic cancer mouse model, characterized by the secretion of the chemokines CCL17 and CCL22, the use of a CCR4 antagonist (CCR4-351) has shown significant effects in disrupting the CCR4-CCL17/CCL22 chemotactic axis, which effectively blocks the recruitment of Tregs to the TME (91). This evidence concerns the gene CCL22 and pancreatic neoplasm.