Secretion of miR-16-5p from uSC-EVs ameliorated glucose-induced podocyte injury by targeting VEGF signalling, whereas administration of miR‐16‐5p-uSCs led to a decrease in the levels of kidney VEGFA, TGF-β1, and pro-inflammatory mediators (MCP-1, TNF-α), which were increased following the establishment of DN. The gene discussed is CCL2; the disease is liver dysplastic nodule.