However, relying on AMPKα2-/- mice, our study firstly demonstrated that the inhibition of Sens2 on mTORC1/p70s6k activation was via an AMPK-dependent manner in pressure overload-induced pathological cardiac hypertrophy, because Sesn2 overexpression could not depress mTORC1/p70s6K signaling pathway in AMPKα2-/- mouse heart. This evidence concerns the gene SESN2 and cardiac hypertrophy.