GSK3β phosphorylation was increased, which in turn mediated GATA4 translocation into the nucleus.87 Akt1-deficient mice were resistant to exercise- or IGF-1-induced cardiac hypertrophy but were sensitized to pressure overload- or ET-1-induced hypertrophy.93 These data indicated that Akt1 had differential regulatory effects on pathological and physiological cardiac hypertrophy. This evidence concerns the gene GSK3B and cardiac hypertrophy.