In contrast, CCL5, CXCL9, and CCL10 were upregulated in the low-risk group; high expression levels of CXCL9 and CXCL10 were correlated with improved OS in most tumors, and anti-PD1 therapy was not beneficial in CXCR3−/− (receptor of CXCL9 and CXCL10) tumor-bearing mice [43]. This evidence concerns the gene CXCR3 and neoplasm.