AKT has been shown to phosphorylate serine‐9 of GSK3β, thereby inactivating the enzyme.12 As we expected, the phosphorylations of AKT and GSK3β were increased in response to stimulation of AngII in Flag‐control cells, indicating that the AngII‐induced decreased activity of GSK3β result in NFATc4 accumulated in the nuclear and promoted the development of cardiac hypertrophy, whereas FKBP12.6 overexpression significantly ameliorated such alterations. This evidence concerns the gene AKT1 and cardiac hypertrophy.