Pressure-induced pathological cardiac hypertrophy is orchestrated by calcineurin–nuclear factor of activated T cells pathway, Janus kinase–signal transducers, and activators of transcription pathway, Pi3K–Akt, MAPK/Erk1/2, canonical Wnt, and G-protein-coupled receptor signaling cascades [2,3], whereas physiological hypertrophy is accompanied by increased Pi3K–Akt and AMPK signaling activities [5]. Here, AKT1 is linked to cardiac hypertrophy.