It has been reported that hyperhomocysteinemia can enhance cisplatin toxicity in renal tubular epithelial cells by inducing endoplasmic reticulum stress and decreasing AKT activity47; elevated adenosine is also involved in cisplatin-induced nephrotoxicity by increasing renal vasoconstriction and thereby decreasing glomerular filtration48. Here, AKT1 is linked to hyperhomocysteinemia.