In conclusion, our study demonstrates that the underlying mechanisms by which mUC-MSC paracrine attenuates renal fibrosis in DN involve blocking TGF-β1-triggered MFT, inhibiting mesangial cell proliferation mediated by the PI3K/Akt and MAPK signaling pathways, and elevating the levels of MMPs in mesangial cells. The gene discussed is TGFB1; the disease is liver dysplastic nodule.