In line with our previous study showing that upregulation of Arg2 was able to activate Akt in endothelial cells, resulting in suppression of endothelial autophagy[28], arginase inhibitor BEC treatment prevented Arg2 overexpression-induced Akt activation in melanoma cells, indicating that this process is associated with the metabolism of its substrate L-arginine. This evidence concerns the gene AKT1 and melanoma.