Measuring β-arrestin recruitment, using CHO cells transfected with human CMKLR1, α-NETA had an IC50 of 0.38 μM. In experimental autoimmune encephalomyelitis, a model for human multiple sclerosis, α-NETA significantly delayed the onset of the disease in agreement with that seen in CMKLR1-deficient mice. This evidence concerns the gene CMKLR1 and multiple sclerosis.