During LM in breast cancer, activated HSCs retain and render natural killer cells quiescent, thus suppressing immune surveillance and licensing the re-emergence of disseminated tumor cells through secretion of CXCL12; [20] HSCs play an important role in LM in colon cancer cells by the SDF-1/CXCR4 axis and provide preclinical evidence that blockade of the axis is a target for antimetastasis therapy [19]. This evidence concerns the gene CXCR4 and colonic neoplasm.