We analyzed LPAs and autotaxin in a cross sectional population of MS patients and in mice in the experimental autoimmune encephalomyelitis model (EAE), using immunization-evoked primary progressive and relapsing-remitting EAE, spontaneous EAE, and EAE in Lpar2 deficient mice, the latter to assess functional implications of LPA signaling and LPAR-dependent immune cell redistribution. This evidence concerns the gene ENPP2 and experimental autoimmune encephalomyelitis.