In WT mice and rats, pathological cardiac hypertrophy and the associated enhancement of mTORC1 activity were observed following chronic AngII stimulation, whereas TR3-KO mice and TR3-KD rats in which TR3 was specifically knocked down in the left ventricle demonstrated attenuated cardiac hypertrophy and diminished mTORC1 activity. This evidence concerns the gene AGT and cardiac hypertrophy.