Overall, we confirmed that 15-R-LxA4, which is reported to be decreased in AD9, was reduced in APP/PS1 mice, and that the elevation of SphK1 increased COX2 acetylation-derived 15-R-LxA4 secretion, suggesting the potential therapeutic use of SphK1 in AD. The gene discussed is SPHK1; the disease is Alzheimer disease.