It is worth mentioning that in the ‘microglia hypothesis’ of schizophrenia, the disease occurs in MS patients with a prevalence (> 60%) of associated frontotemporal lesions [97, 98], a pathogenesis supported by the demonstrated CCL2-driven microgliosis observed in the neocortex of EAE-affected mice. This evidence concerns the gene CCL2 and myeloid sarcoma.