For example, in a pancreatic cancer model of combination immunotherapy, T-cells were localized to tumor microenvironment stroma and addition of CXCR4 small molecule inhibitor AMD3100 led to T-cell redistribution and rapid accumulation near tumors, enhancing the antitumor efficacy of an anti–PD-L1 mAb combination regimen [7]. The gene discussed is CXCR4; the disease is pancreatic neoplasm.