Collectively, the results of this work were in the same line as the aforesaid findings, as the nephropathy group showed a marked downregulation in the expression of the antifibrotic markers mir-29b, mir-181, Let-7b, and Smad-7 and upregulation in the profibrotic one, Smad-3, TGF-β, and Coli-1, which improved with Br-MSCs + EXOs, EOXs, and Br-MScs, respectively. This evidence concerns the gene TGFB1 and kidney disorder.