Accordingly, we demonstrated that the CXCR4 pathway correlated with the expression of the mesenchymal marker vimentin in luminal B primary tumors and that the overexpression of CXCR4 in metastatic SLNs was concurrent with that of other EMT-related genes, such as SNAI2, TGFB2, and TWIST1. Thus, our results provide an important evidence for the association of CXCR4/CXCL12 axis with the progression of tumor cells toward a mesenchymal phenotype, suggesting a potential mechanism that drives the metastatic spread of luminal B BC cells from primary tumors and SLNs to distant sites. This evidence concerns the gene CXCL12 and neoplasm.