These negative results can be explained by the fact that the electroporation with S6K1 plasmid was not sufficient to generate a hypertrophic signal to counteract cachexia as AET did (see Figure 2 and Figure S2), because to display its functions S6K1 needs to be activated by phosphorylation from high-level stimuli into the Akt/mTORC1 pathway. The gene discussed is AKT1; the disease is Cachexia.