NFKB1 and liver dysplastic nodule: Chen et al. (2014) observed an interaction between elevated SP1 and NFκB-p65 within the podocyte nucleus upon exposure to high glucose. Furthermore, they identify the direct binding between SP1 and the DNMT1 promoter region, indicating the SP1/NFκB p65-Dnmt1 pathway may be a therapeutic target for protecting against podocyte injury in DN (Zhang et al., 2017).