On the other hand, the physiological cardiac hypertrophy is mediated via the activation of tyrosine kinase receptors by growth hormone (GH) and insulin-like growth factor I (IGF-I) that culminates in triggering the phosphoinositide 3-kinase–RAC-α serine/threonine-protein kinase enzyme and Akt (PI3K–AKT) [6]. This evidence concerns the gene AKT1 and cardiac hypertrophy.