The co-localization of Nav1.6, the Na+/Ca2+ exchanger (NCX), and markers of axonal injury has led to the hypothesis that the persistent influx of Na+ through Nav1.6 channel in MS, and in the EAE animal model of MS, causes the NCX to operate in reverse, leading to the toxic accumulation of intracellular Ca2+ ions that results in cell death and axonal degradation [10, 22, 30, 31]. The gene discussed is SLC8A1; the disease is myeloid sarcoma.