Our results can be summarized as follows: (1) AT could attenuate cardiac hypertrophy and cardiac fibrosis in response to pressure overload in vivo; (2) the effects of AT could be mediated by mitogen-activated protein kinase 1/2 signaling pathway; (3) AKT signaling pathway also participated in the protective role of AT on pathological cardiac hypertrophy; and (4) GATA4 was also reduced after AT stimulation in response to TAC. Here, MAP3K1 is linked to ataxia telangiectasia.