Studies have demonstrated that the activation of AMPK inhibits protein synthesis and the development of cardiac hypertrophy via a number of pathways, such as eukaryotic elongation factor-2 (eEF2), p70S6 kinase, and mammalian target of rapamycin (mTOR) (Proud, 2004) AICAR, as an agonist of AMPK, can activate phosphorylation of AMPK-α catalytic subunits (Thr172) to prevent cardiac hypertrophy induced by phenylephrine (Huang et al., 2014). This evidence concerns the gene MTOR and cardiac hypertrophy.