Unlike most previous PDAC biomarker studies that have investigated either serum tumor markers (e.g., CA19-9 and CEA) or genetic variants in isolation, our work uniquely integrates PD-1/PD-L1 polymorphisms with their soluble protein counterparts within the same patient cohort, offering a plausible biological mechanism for the observed genetic risk. Here, CEACAM5 is linked to neoplasm.