SCN8A and myeloid sarcoma: 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).