The authors targeted the delivery of antagonists and the disruption of CXCL12/CXCR4 signaling in the tumor tissue, which promoted depletion of the stromal barrier and relieved immunosuppression, and the T cell infiltration into the tumor site, enhancing the efficacy of immune checkpoint blockade therapy in TNBCs [50]. The gene discussed is CXCR4; the disease is neoplasm.