Partial toxin‐induced depletion of FAP+ CAFs, as well as pharmacological blockage of CXCL12 signaling by inhibiting its receptor C‐X‐C chemokine receptor 4 (CXCR4), reduced tumor growth and enhanced T cell accumulation within the tumor, thus sensitizing tumors to α‐PDL1 treatment. Here, CXCL12 is linked to neoplasm.