Tumor cell‐derived PGE2 drives immune evasion by disrupting communication and inducing dysfunction in conventional dendritic cells (cDCs), NK cells, and cytotoxic T cells, while its metabolite 15‐keto‐PGE2 enhances the immunosuppressive activity of regulatory T cells.[24, 65, 66, 73] Bulk RNA‐seq revealed that human NK cells predominantly express the PGE2 receptors PTGER2 (EP2) and PTGER4 (EP4), with Dex selectively upregulating PTGER2 expression (Figure 5E). The gene discussed is PTGER4; the disease is neoplasm.