Based on our findings of a tumor cell-derived CCL26 and CX3CR1+ PMN-MDSCs interaction axis in GC, we propose that this pathway holds translational potential both as a noninvasive biomarker for stomach carcinogenesis, potentially reducing the need for repeated endoscopic examinations, and as a therapeutic target to disrupt tumor-myeloid cross-talk, thereby limiting immunosuppression and tumor progression. This evidence concerns the gene CCL26 and neoplasm.