However, VPAC1 signaling is also linked to neuroprotection [50]; therefore, it cannot be excluded that the increased VPAC1 expression in the reported MS cases reflects the homeostatic neuroprotective response of stressed axons trying to retain functionality in a non-physiological CNS microenvironment, such as in the NAWM of MS patients. This evidence concerns the gene VIPR1 and myeloid sarcoma.