In other studies, febuxostat has been shown to exert an anti-inflammatory action and protect against diabetic nephropathy development in KK-Ay obese diabetic mice [31], reduce ER stress through the upregulation of SIRT1-AMPK-HO-1/thioredoxin expression [32], inhibit TGFβ1-induced epithelial–mesenchymal transition via downregulation of USAG-1 expression in Madin–Darby canine kidney cells in vitro [33], and slow the development of nephropathy in experimental type 2 diabetes via the reduction of uric acid, renal oxidative stress, and inhibition of profibrotic signaling [34]. This evidence concerns the gene TGFB1 and type 2 diabetes mellitus.