In fact, optional targets for treating HCC in a DEN-induced model are mainly confined to inflammatory response pathways (e.g., toll-like receptor 4 and IL-6).23 Hence, a rapid HCC model established by hydrodynamic transfection of activated forms of AKT (myr-AKT) and c-Met (V5-c-Met) into the FVB mouse liver is employed here for evaluating the effects of celastrol on the process of HCC formation. The gene discussed is AKT1; the disease is hepatocellular carcinoma.