(120) reported that catalpol could effectively inhibit oxidative stress and inflammation in HFD/STZ-induced DN mice and in a high-glucose–induced podocyte model, and that the mechanism may be related to the AMPK/SIRT1/NF-κB pathway, indicating that catalpol has potential value in the treatment of DN. Here, NFKB1 is linked to liver dysplastic nodule.