As a lethal complication of diabetes mellitus, diabetic nephropathy is ameliorated by AS-IV through the inhibition of extracellular signal-regulated kinase 1 and 2 (Erk1/2), nuclear factor kappa B (NFκB), and protein kinase B (Akt)/ mammalian target of rapamycin (mTOR) signaling pathways in mice model [15]. This evidence concerns the gene AKT1 and diabetes mellitus.