Specifically, we have shown that unlike hypertension-induced and ischemia-induced models (36, 44, 45, 46, 47), the cardiac hypertrophy triggered by CPT2 deficiency is resistant to attenuation by rapamycin, an mTor inhibitor, and by trichostatin A, a deacetylase inhibitor (23). This evidence concerns the gene MTOR and cardiac hypertrophy.