The dual defect of BATF3-/- mice in priming Tregs and effector T-cells that express CXCR3 and in generating chemokine gradients for T-cell recruitment to infected tissues provided a strong rationale for blocking the interaction of CXCR3 with its ligands with a neutralizing antibody in the MC38 tumor model and during H. pylori infection. This evidence concerns the gene BATF3 and neoplasm.