Instead, it is now clear that the immunomodulatory effects associated with the use of selective EP4 antagonists in experimental studies cannot be achieved by the general inhibitors of prostaglandin synthesis (i.e., NSAIDs, either non-selective or selective COX-2 inhibitors), nor can they be achieved with selective antagonists for other prostanoid receptors, as also reflected by results from studies of arthritis models in EP4- vs EP(1–3)-knockout mice [18]. Here, PTGS2 is linked to arthritic joint disease.