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. This evidence concerns the gene MAP1LC3A and diabetic kidney disease.