Accordingly, although antibodies to KV1.1 and 1.2 subunit labelled numerous JXPs in cuprizone-treated mice, many of these specializations were greatly elongated with KV1 proteins present in internodes, consistent with earlier documented dislocation of axonal K+ channels from their canonical sites in demyelination animal models and MS brain [49], [50]. The gene discussed is KCNA1; the disease is myeloid sarcoma.