BECN1 and diabetic kidney disease: Experiments have shown that both chronic high blood glucose levels (88), and the accumulation of AGEs (91), as well as the knockout deletion of autophagy-related genes (Atg5-12/Beclin-1/LC-3) (84–86, 96), eventually lead to damage of renal podocytes and proximal tubular epithelial cells by inhibition of autophagy, which in turn causes renal inflammation, fibrosis, proteinuria, and other symptoms of diabetic nephropathy.