Moderate (five-fold) overexpression of SIRT1 in mice protects them from age-related cardiac hypertrophy, but a pronounced (12-fold) overexpression may enhance the hypertrophy (Alcendor et al., 2007) through deacetylation of PH domain of Akt kinase and PDK1 protein, enhancing Akt-dependent intracellular signaling, promoting mitosis and cardiomyocyte proliferation which can directly lead to cardiac hypertrophy (Sundaresan et al., 2011). This evidence concerns the gene AKT1 and cardiac hypertrophy.