Indeed, the PGE2–EP2/EP4 axis restricted antigen-specific T cell expansion in response to IL-2, and this effect was remarkably rapid and durable in vitro, suggesting that within the TME, cell niches with high local levels of PGE2 might swiftly engage and induce IL-2 anergy in approaching tumour-reactive cytotoxic CD8+ T cells, quickly collapsing their bioenergetics, thereby suppressing their expansion, and ultimately compromising the survival of these clonotypes. Here, IL2 is linked to neoplasm.