We have showed that hPMSCs could mitigate the hepatic pathological damage in the GVHD mouse model by maintaining the balance in redox metabolism in tissues, as well as mononuclear cells, and CD4+IL-10+ T cells, which were associated with the enhancement of Nrf2 activation and attenuation of NF-κB activation and the inhibition of PD-1 expression in CD4+IL-10+ T cells. This evidence concerns the gene CD4 and graft versus host disease.