To further explore the mechanism underlying the antifibrotic effect of GDNF-AMSCs, we evaluated whether the therapeutic effect of GDNF-AMSCs on renal fibrosis was regulated by inhibiting oxidative gp91-phox and p67-phox, oxidative markers, which are the major sources of ROS and play the important role in generating superoxide and subsequently contribute to cell damage. This evidence concerns the gene CYBB and renal fibrosis.