Hence, our results revealed that the for MS relevant inflammatory mediators IFN-γ, and to a lesser extent TNF-α, increased TG2 expression in OPCs, though no apparent correlation between cytokine-induced TG2 expression and increased OPC differentiation at the immature OLG stage exists, as was observed upon sustained expression of hTG2 in OLGs (Figure 5). The gene discussed is TGM2; the disease is myeloid sarcoma.