In mouse models of ureteral obstruction and aristolochic acid nephropathy, as well as in HK-2 cells, ginsenoside Re treatment suppresses autophagy and reduces TGF-β-stimulated profibrotic markers, thereby mitigating fibrotic injury and preserving kidney function (Liu Y. Y. et al., 2024). This evidence concerns the gene TGFB1 and Balkan nephropathy.