The activation of CXCR4/CXCL12 signaling can further stimulate its downstream phosphatidylinositol-4,5‐bisphosphate 3‐kinase (PI3K)/ protein kinase B (PKB/AKT) and mitogen-activated protein kinases (MAPK) signaling pathways, leading to protumoral changes such as angiogenesis, extracellular matrix remodeling, establishment of pre-metastatic niche, recruitment of CXCR4+ tumor cells, and polarization of the immune microenvironment toward an immunosuppressive one [7, 8]. This evidence concerns the gene CXCR4 and neoplasm.