In conclusion, although further studies are required to validate the molecular mechanisms and the association between the expression of these EMT- and immune-related markers and BC progression, our findings suggest that the upregulation of the CXCR4/CXCL12 axis and the presence of protumor macrophages in the primary tumor and SLNs sustain the aggressiveness of luminal B BC cells, favoring the generation of a permissive tumor microenvironment and leading to metastatic spread. The gene discussed is CXCL12; the disease is neoplasm.