Considering that in MS patients inflammation declines with disease duration while neurodegeneration proceeds and activated microglia persists in all lesions in progressive MS, using the MOG–EAE model there was the need to answer the question of anti-HuR ASO effects resulted from a direct mechanism on myelination or indirectly through a central immune/inflammatory suppression. The gene discussed is ELAVL1; the disease is myeloid sarcoma.