Depletion of NUP160 restored autophagy and inhibited inflammation and fibrosis in high glucose (HG)-treated NRK-52E cells and STZ-induced DN mice by downregulating the expression of p62 and Collagen IV (Col-IV), increasing the ratio of LC3II/LC3I, and inactivating nuclear factor (NF)-κB signaling. The gene discussed is NFKB1; the disease is liver dysplastic nodule.