COX-2 mediated promotion of migratory [23], invasive [24], SLC stimulatory [25] and VEGF-C and –D up-regulatory [25–27] functions were primarily due to activation of the PGE receptor EP4 expressed by breast cancer cells [26, 27] as well as tumor infiltrating macrophages [25], suggesting that both COX-2 and EP4 are good therapeutic targets for abrogating all these PGE2 mediated functions. Here, PTGS2 is linked to neoplasm.