Notably, their functional annotation and pathway enrichment profiles suggest that these genes collectively may drive key pathogenic processes in DN, including extracellular matrix remodeling and fibrosis (COL1A2, FN1), immune cell recruitment and chronic inflammation (CCL2, CD163), oxidative stress–induced injury, and metabolic reprogramming of renal parenchymal cells under hyperglycemic stress. This evidence concerns the gene COL1A2 and liver dysplastic nodule.