TGFB1 and myeloid sarcoma: We proposed that the chronic overexpression of TGFB1, while efficiently containing acute inflammation in MS spinal cords, may promote astrocytosis, partial demyelination and low grade chronic inflammation via at least two main mechanisms: (i) the astrocytic synthesis of profibrotic extracellular matrix proteins [15] and (ii) a direct inhibitory effect of TGFB1 on both myelin synthesis [13] and oligodendrogenesis [16].