Pro-fibrotic genes were upregulated in the aTAL including ZEB1, LAMC2, and SMAD3. FHL2 is known to mediate podocyte dedifferentiation and glomerular basement membrane thickening in diabetic kidney disease and is pro-fibrotic in the TI through the beta-catenin pathway35–37, aligning with extracellular matrix-associated pathways enriched in the aTAL enrichment analysis for top 300 DEGs. This evidence concerns the gene LAMC2 and diabetic kidney disease.