Ptgs1/Ptgs2-/- tumor models have implicated tumor-resident NK cells as important sources of the chemokines required for optimal cDC1 recruitment into solid murine tumors, and similar correlative data from human solid cancers, such as melanoma, breast cancer, and lung cancer, also support this NK cell/XCL1 axis as a driver of cDC1 infiltration [17]. The gene discussed is PTGS1; the disease is neoplasm.