[37] used immortalized podocytes and adriamycin-induced FSGS mouse models to confirm that baicalin improves the FSGS process by reducing podocyte damage and revealed the potential mechanism by which baicalin inhibits the NOTCH1-snail axis-mediated podocyte epithelial-mesenchymal transition (EMT).These results support the key biomarkers screened in this study. Here, SNAI1 is linked to focal segmental glomerulosclerosis.