Increased levels of hyaluronan are observed in both EAE lesions and in areas of complete demyelination in MS, perhaps due to altered hyaluronan synthesis, partial hyaluronan degradation, or particular stimulation of TLR2 on oligodendrocytes, events necessary to perform an adequate remyelination blockade [59, 60]. The gene discussed is TLR2; the disease is myeloid sarcoma.