At the cellular level, the ability of thyroid hormones to induce myocardial hypertrophy has been explained by the activation of PI3K/AKT/mTOR and GK3β signaling pathways and an increased protein synthesis in the terminally differentiated cardiac myocyte, particularly sarcoplasmic reticulum Ca2-ATPase and myosin heavy chain [6,11,47]. This evidence concerns the gene MTOR and cardiac hypertrophy.