Importantly, Ptgs1/Ptgs2−/− tumors were able to grow in Rag1−/−, Tap1−/−, and Batf3−/− hosts (Figures 4A and 4B), indicating that prostanoid deficiency did not impair tumor formation in a cell-intrinsic fashion but rather acted to prevent CD8α+/CD103+ DC-dependent rejection mediated by CD8+ T lymphocytes. This evidence concerns the gene PTGS1 and neoplasm.