Our results showed that depletion of NUP160 restored autophagy and inhibited inflammation and fibrosis in HG-treated NRK-52E cells and STZ-induced DN mice by downregulating the expression of p62 and Col-IV, increasing the ratio of LC3II/LC3I, and inactivating NF-κB signaling Moreover, NUP160 knockdown could ameliorate pathological damage in DN mice. The gene discussed is NUP160; the disease is liver dysplastic nodule.