The development of DN is stimulated by sustained hyperglycaemia [2], and its key pathologic features include gradual thickening of the glomerular basement membrane (GBM) and glomerular hypertrophy accompanied by mesangial matrix expansion with accumulation of several matrix proteins, such as collagen type I, laminin β1, and fibronectin [2]. Here, FN1 is linked to liver dysplastic nodule.