For example, blockade of PGE2‐EP4 receptor signalling by pharmacological (e.g. COX inhibitors and EP4 antagonists) or genetic approaches (e.g. KOs of mPGES1 or EP4 genes) suppressed myelin oligodendrocyte glycoprotein peptide‐induced experimental autoimmune encephalomyelitis (EAE) and reduced Th1 and Th17 cell development, and these suppressing effects were further enhanced by co‐inhibition of EP2 receptors (Kihara et al., 2009; Yao et al., 2009; Esaki et al., 2010). The gene discussed is PTGER4; the disease is experimental autoimmune encephalomyelitis.