Contrary to previous reports indicating that high glucose and high osmolality diminish the interaction between IκBα and SUMO1, reduced SUMOylation of IκBα leads to decreased expression levels of IκBα, resulting in the activation of NF-κB signaling, which is implicated in the pathogenesis of diabetic nephropathy (DN). The gene discussed is NFKBIA; the disease is diabetic kidney disease.