In this regard, TGF-β1 might induce astrogliosis and trigger an OL-defective genetic program in MS patients [17,18], although it might also reduce the neuroinflammatory response in MS patients and diminish the activation of B-lymphocytes in the experimental autoimmune encephalomyelitis (EAE) model of MS [17,19]. This evidence concerns the gene TGFB1 and myeloid sarcoma.