Accordingly, in a mouse model, generated by hydrodynamic gene transfer, leading to the overexpression of both activated AKT and neuroblastoma Ras viral oncogene homolog (N-Ras) in the liver, AKT and N-Ras expression accelerated much more HCC development by activating the mammalian target of rapamycin complex 1 (mTORC1) than the overexpression of AKT alone [75]. This evidence concerns the gene NRAS and hepatocellular carcinoma.