Although we have not directly demonstrated this using ultrastructural analysis, conditional murine knockouts of the paranodal proteins Caspr1, Nf155, βII spectrin, and 4.1.B [20–24] showed a lack of tight septate junctions and an increased peri-axonal space at the ultrastructural level, which was associated with an elongation of the paranodal protein profiles and dislocation of the juxtaparanodal voltage-gated channels Kv1 towards the PNJ, similar to that seen in MS tissue. This evidence concerns the gene CNTNAP1 and myeloid sarcoma.