However, after depletion of fibroblast activation protein (FAP)+ stromal cells producing CXCL12 in the tumor, immune control of PDAC growth could be achieved by the synergistic action of a CXCL12 receptor chemokine (C-X-C motif) 4 inhibitor and anti-PD-L1 [43], an approach that is currently tested in a clinical Phase 2 trial for patients with metastatic pancreatic cancer. The gene discussed is CXCL12; the disease is neoplasm.