Experimental animal models and clinical data support the notion that LPA can be protective in inflammatory diseases: In the murine experimental autoimmune encephalomyelitis model of multiple sclerosis (MS) and in MS patients, concentrations of several LPA species are reduced, and subsequent deficiency in LPAR2 signaling in immune cells promotes disease progression [32]. This evidence concerns the gene LPAR2 and experimental autoimmune encephalomyelitis.