The possible mechanisms of AM in the treatment of diabetic kidney disease (DKD) could be alleviating the early glomerular pathological changes via inhibiting Akt/mTOR/p70S6K signaling, ameliorating inflammation by the inhibition of iRhom2/TACE signaling, improving lipid disorders by enhancing PPARα/γ, protecting ER stress and suppressing the expression of TNF-α and TGF-β1 [33–36]. This evidence concerns the gene AKT1 and diabetic kidney disease.