Hypertrophic stimuli such as isoproterenol and PE led to GSK3β phosphorylation.95 Overexpression of active GSK3β attenuated cardiac hypertrophy induced by pressure overload or chronic β-adrenergic stimulation.96 In addition to transcription factor regulation, another well-established downstream effector of Akt is mTOR. The gene discussed is GSK3B; the disease is cardiac hypertrophy.