Furthermore, levels of prostaglandin E2 (PGE2), a lipid signaling molecule involved in pain and inflammation, are elevated in the brain of MCAO mice, and deletion of its upstream synthetase, microsomal prostaglandin E synthase-1 (mPGES-1) effectively inhibits PGE2 synthesis and reduces brain infarction [110], whereas FABP5 precisely regulates mPGES-1 expression by controlling the binding of NF-κB to the binding site in the mPGES-1 promoter [109]. The gene discussed is PTGES; the disease is brain infarction.