In addition, other players in the TME, including growth factors, inflammatory cytokines, and extracellular matrix enzymes, and the impact of the tumor on the microenvironment, such as induction of hypoxia, influence the CXCR3 axis and add yet another level of complexity to CXCR3-regulated processes, ultimately making the outcome of potential blockade hard to predict. This evidence concerns the gene CXCR3 and neoplasm.