CXCR2+ MDSCs promote breast cancer progression by directly inducing cancer cell epithelial-mesenchymal transition and indirectly promoting T-cell exhaustion by upregulating the expression of immunosuppressive molecules Tim-3, PD-1, PD-L1, LAG-3, and CTLA-4 on CD4+ or CD8+ T cells and inducing exhaustion of the activated T cells via IFN-γ (72). Here, HAVCR2 is linked to cancer.