Additionally, hypertrophic signals (such as pressure overload, β-adrenergic stimulation and angiotensin II) can also induce mTORC1 signaling in the heart, resulting in significant phenotypic impact: mTORC1 can induce cardiac hypertrophy as a compensatory mechanism to maintain function during pressure overload but also, and depending on the molecular background, can induce pathological cardiac hypertrophy [69]. This evidence concerns the gene AGT and cardiac hypertrophy.