Besides high glucose (HG) treatment, hMCs were also stimulated with tunicamycin (TM) and thapsigargin (TG) as well as transforming growth factor β1 (TGFβ1) and tumor necrosis factor α (TNFα) to mimic diabetes evoked endoplasmic reticulum (ER) stress or the increased release of profibrotic or proinflammatory molecules to address multiple aspects of DKD [34]. This evidence concerns the gene TNF and diabetic kidney disease.