Given the suggested LPA effects in endothelial physiology [8, 34], the increased BBB permeability upon EAE development [2, 3], and the observations made here that ATX/LPA peak in the plasma earlier than in the spinal cord, it is tempting to assume that increased amounts of ATX/LPA could be extravasated in the CNS, possibly contributing to local LPA levels and promoting disease (EAE/MS) pathogenesis. This evidence concerns the gene ENPP2 and myeloid sarcoma.