This study identified CXCR4 as a novel direct target of transcriptional activation by KLF8 and a key mediator of KLF8's role in promoting CXCL12-dependant beast cancer cell migration and invasion required for the invasive growth of the primary tumor as well as TEM essential for the lung metastasis involving a feed-forward activation of FAK (Figure 8). This evidence concerns the gene CXCL12 and neoplasm.