In a mouse model of diabetic nephropathy, inhibition of miR-21 improved kidney function and alleviated the progression of renal injury [42], whereas inhibition of renal miR-192 suppressed the expression of fibrotic markers, such as collagen, TGF-β1, and fibronectin in a mouse model of type I diabetes nephropathy [43]. This evidence concerns the gene FN1 and diabetic kidney disease.