High glucose can stimulate EGFR transactivation, which has been reported to occur in the pathogenesis of renal fibrosis in DN via the ERK, STAT3, AKT and TGF‐β/Smad3 pathways4, 5, 6, 30; however, the mechanism of sustained EGFR activation is unclear. This evidence concerns the gene STAT3 and liver dysplastic nodule.