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In this study, we precisely define what cells produce CCL20 in pancreatic inflammation and cancer. Through analysis of single cell RNA data, mutation and copy number signatures, gene methylation, and\n                  <jats:italic>in vitro<\/jats:italic>\n                  studies, we show that CCL20 and other NF-\u03baB driven chemokine production is largely dependent on oncogenic KRAS in the malignant pancreas. Blockade of CCL20-CCR6 signaling\n                  <jats:italic>in vivo<\/jats:italic>\n                  using a novel partial agonist inhibitor, CCL20LD, increased recruitment of antigen presenting cells without significantly impinging tumor growth. Lastly, resistance to pan-RAS or allele-specific KRAS inhibitors decreased CCL20-dependent immune recruitment in culture. These results suggest that oncogenic KRAS activates NF-\u03baB signaling in human pancreas cancer, resulting in pharmacologically reversible changes to chemokine production that may participate in immune suppression or immune evasion within the pancreas cancer microenvironment.\n                <\/jats:p>","DOI":"10.64898\/2026.04.13.717530","type":"posted-content","created":{"date-parts":[[2026,4,15]],"date-time":"2026-04-15T22:30:16Z","timestamp":1776292216000},"source":"Crossref","is-referenced-by-count":1,"title":["Mutant KRAS promotes NF-\u03baB driven CCL20 chemokine expression in pancreatic ductal adenocarcinoma"],"prefix":"10.64898","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-2940-3511","authenticated-orcid":false,"given":"Donovan","family":"Drouillard","sequence":"first","affiliation":[{"name":"Department of Microbiology & Immunology; Medical College of Wisconsin, Milwaukee WI, USA"},{"name":"Center for Immunology; Medical College of Wisconsin, Milwaukee WI, 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