CXCL16 and neoplasm: In a similar mammary carcinoma mouse model, IR (12 Gy × 2 fractionation dose) together with CTLA-4 blockade induced the secretion of CXCL16, which could bind to CXCR6 on the surface of Th1 cells and co-stimulate the CD8+ T cells to be recruited to the tumor sites, resulting in the regression of the primary tumor and metastases [79].