Despite these, up to present, there are still some important issues unresolved in the role of glomerular injuries in DN at the early stage treated by HKC, for instance, whether HKC can improve glomerular hypertrophy, GBM thickening and mild mesangial expansion by means of targeting PI3K/Akt/mTOR pathway and its signaling activity, and if yes, what are the underlying therapeutic mechanisms involved in vivo and in vitro. This evidence concerns the gene MTOR and liver dysplastic nodule.