It has already been reported that JAK/STAT was upregulated in glomerular from patients with early DKD and tubulointerstitial expression of various JAK and STAT isoforms increases with disease progression and is inversely correlated with eGFR.[59] NF-kB is a key transcription factor activated by cytokines and oxygen radicals during renal inflammation in diabetes and is activated through JAKs/STATs, leading to the structural alterations and functional abnormalities in DKD.[60] In renal cells, NF-kB is rapidly activated by multiple stimuli, including hyperglycemia, AGEs.[61]. This evidence concerns the gene SOAT1 and diabetic kidney disease.