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. The gene discussed is GDNF; the disease is renal fibrosis.