In addition to the above-mentioned role of tumor-derived exosomes, HPV infection generates cervical cancer cells that secrete CXCL10 and CXCR3 complexes binding to fibroblasts and activating the JAK/STAT pathway, which leads to the upregulation of the exosomal programmed death-ligand 1 (PD-L1), creating resistance to cell death (Figure 2) and forming an immune escape response pathway that leads to tumor emergence [53]. This evidence concerns the gene CXCR3 and neoplasm.