Previous studies showed that miR-21 prevented hypertrophy by targeting the phosphatase and tensin homolog/phosphatidylinositol-4,5-bisphosphate 3-kinase/Protein kinase B (PTEN/PI3K/Akt) pathway in vivo and in vitro, and over-expression of PTEN may act as an originator or modulator of diabetic nephropathy [146]. Here, AKT1 is linked to diabetic kidney disease.