In comparative transcriptome studies, SP1 was identified as a shared TF in both human DN and the eNOS−/− db/db mouse model of DN.21 SP1 has been previously reported to play a role in the profibrotic pathway during the progression of mesangial expansion and glomerulosclerosis by promoting the transcription of TGF-β and extracellular matrix.22 However, these genes were less upregulated than the dynein genes in human DN15 and were not significantly correlated with hyperglycemia in rodent models of DN,21 suggesting a different mechanism underlying the early pathophysiology of DN. Here, TF is linked to liver dysplastic nodule.