In this present study, EGCG treatment at 40 mg/kg dosages significantly down-regulated the amount of p-AKT to Akt, p-mTOR to mTOR, and p-ERK to ERK, which indicated that the Akt/mTOR signal pathway was involved in the EGCG treatment process for cardiac hypertrophy, and the alleviation of hypertrophy induced fibrosis may also be associated with the inhibition of Akt/mTOR signal pathway. This evidence concerns the gene MTOR and cardiac hypertrophy.