Although previous studies have reported that PP2A protects noncardiac cells against oxidative stress in vitro [38], and PP2A negatively regulates the hypertrophic response and cardiomyocyte specific deletion of PP2A causes cardiac hypertrophy [39, 40], suggests PP2A may play a protective role in the cardiac hypertrophy progression, the detailed mechanism of PP2Acα in cardiac oxidative stress and hypertrophy is unclear, here we demonstrates the key pathway that PP2Acα regulated in this process, and first find REGγ plays role in cardiac hypertrophy by targeting PP2Acα. This evidence concerns the gene PTPA and cardiac hypertrophy.