AKT1 and diabetic kidney disease: To investigate the role of lncRNA SOX2OT and tissue inhibitor of metalloproteinase 3 (TIMP3) in the progression of DKD, overexpression or gene deletion was used in treated mice and mouse mesangial cells, suggesting that the overexpression of lncRNA SOX2OT (SOX2 overlapping transcript) restored autophagy via AKT/mTOR, while TIMP3 deletion led to reduced FOXO1 expression of the autophagy key factor and increased expression of the FOXO1 transcriptional repressor STAT1, driving renal function to deteriorate in DKD patients and mice (Fiorentino et al., 2013; Chen K. et al., 2021).