Hence, we may hypothesize that (−)-epigallocatechin 3-O-gallate could be advantageous against diabetic kidney damage, which correlates with AGEs with or without a receptor-dependent pathway and their related inflammatory responses, and then (−)-epigallocatechin 3-O-gallate subsequently suppresses the induction of mesangial hypertrophy and fibronectin synthesis in diabetic nephropathy. Here, FN1 is linked to diabetic kidney disease.