Moreover, Ptger4 KO resulted in more robust tumor growth suppression than Ptges KO; s.c. implanted Ptger4-KO tumors were almost universally rejected, while approximately 30% of Ptges-KO tumors escaped antitumor immunity, likely through the residual PGE2 signaling through intact EP4 receptors on tumor cells that according to Figure 2D have a non-redundant role in creating immunosuppressive TME. The gene discussed is PTGER4; the disease is neoplasm.