In addition, our findings that S1pr2-deficient mice or wild-type mice, treated with the S1PR2 antagonist JTE013, exhibited a dramatic decrease in cerebral oedema also raise the intriguing possibility that S1PR2 targeting could be potentially beneficial to prevent the development of malignant MCA syndrome, in which rapid brain oedema following a large MCA infarct leads to herniation and high mortality rates (80%)45, particularly in younger stroke patients46, 47. This evidence concerns the gene S1PR2 and edema.