TGFB1 and myeloid sarcoma: These results are in concordance with previously published findings supporting a mechanism for TGF-β1-induced TGF-β1 release; moreover, more importantly, it also provides evidence to support a possible crosstalk between these two pathways in the CPZ model of MS, in which the TGF-β1 receptor activation might induce the observed recovery of Nrf2 protein expression at the peak of demyelination.