This assumption is further supported by our data showing (i) increased levels of CCL5, CXCL10, and IFNγ in the tumor microenvironment of Ackr2-targeted tumors compared to controls (Figure 2(c)), and (ii) treatment with anti-CCL5-blocking antibodies in mice bearing Ackr2-targeted tumors, but not in those with control-targeted tumors, reverses the inhibition of tumor growth (Figure 2(d)) and decreases the frequency of CD45+, NK, CD8+, and CD4+ effector cells in the TME (Figure 2(e)). This evidence concerns the gene CD8A and neoplasm.