Moreover, since immune desert tumors are enriched in EMT gene-set signatures [27] and considering CXCR4/CXCL12 ability in shaping TME toward immunosuppression [28–32], CXCR4 blockade may potentiate PD-1/PD-L1 immunotherapies by a dual action: reverting cancer cells mesenchymal phenotype on one hand and driving TME polarization toward immune-activation on the other hand. Here, CXCR4 is linked to cancer.