Preclinical studies observed a reduced expression of Nav1.6 in EAE (9). Contributes to the persistent Na+ influx, imbalance of the Na+/Ca2+ pump and, intra-axonal Ca++ accumulation in injured axons in MS. This leads to impaired sodium-calcium exchanger function, may contribute to axonal ephaptic abnormalities, and leads to an activation of damaging injury cascades with consequent neurodegeneration, in the long term (11). Here, SLC24A3 is linked to myeloid sarcoma.