As MTLn3 JP did not show chemotaxis to CXCL12 at any concentration in vitro and we did not observe upregulation of CXCR4 expression in vivo in this control cell line, we believe that the in vivo invasion at high concentration is a result of stimulating macrophages (which express CXCR4 [44-46]) within the tumor microenvironment, which can promote cancer cell invasion through the paracrine loop [21]. This evidence concerns the gene CXCR4 and neoplasm.