CXCR4 and pancreatic neoplasm: Activation of the latter has been reported to generate gemcitabine resistance in PDAC cell lines through an NFκB‐HIF1α‐CXCR4 positive feedback loop49 and/or by increasing MUC4.50 Overexpression of mucins is implicated in chemoresistance in multiple tumors, including MUC1 in pancreatic cancers.26 Thus, we also identified gene pathways whereby gemcitabine treatment itself directly enables resistance mechanisms.