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). Here, PTGER2 is linked to neoplasm.