In light of evidence functionally linking PDAC cell-intrinsic mechanisms (including the KRAS effector MYC49, fatty acid sensor PPARδ50,51 and neutrophil chemoattractant CXCL1 (ref. 11)) to evolution of an immune-suppressive stroma, identifying putatively druggable cancer cell-intrinsic mechanisms that promote this immune-suppressive, treatment-resistant microenvironment has the potential to highlight previously uncharacterized targets for therapeutic intervention and bring much-needed improvement in outcomes to individuals with PDAC. The gene discussed is CXCL1; the disease is cancer.