Although PMD is generally considered non-inflammatory, dys-and demyelinating animal models of PMD caused by gene overexpression (modelling gene duplication in patients, the most common cause of PMD) have overt microglial activation [54, 55] and small numbers of pathogenic CD8 + effector T cells in the CNS [56–58]. The gene discussed is CD8A; the disease is Pelizeaus-Merzbacher spectrum disorder.