While recent data found that KCNA1 gene is downregulated during demyelination in the cuprizone model (Martin et al., 2018), in animal models of MS, Kv1.2 (and also Kv1.1) ectopically redistributes to nodes and internodes of WM axons (McDonald and Sears, 1969; Wang et al., 1995; Sinha et al., 2006; Jukkola et al., 2012; Zoupi et al., 2013; Kastriti et al., 2015), while in human MS, the dislocation of Kv1.2 channels is associated with paranodal pathology, particularly in NAWM regions, and contributes to axonal dysfunction (Howell et al., 2010; Gallego-Delgado et al., 2020). The gene discussed is KCNA2; the disease is myeloid sarcoma.