Additionally, we found that the accumulation of S-adenosylmethionine (SAM), a Met metabolite associated with a decrease in glycine-N-methyltransferase (Gnmt) expression/activation in renal tubular cells, possibly contributes to the activation of mTORC1 and impairment in autophagy and leads to the pathogenesis of DKD in rats with T2DM and obesity. The gene discussed is GNMT; the disease is diabetic kidney disease.