During cardiac hypertrophy, markedly decreased levels of miR-1 and miR-133a mitigate the downregulation of GLUT4 expression by increasing the activity of insulin-like growth factor (IGF-1) and Akt signaling, which promotes the phosphorylation of GLUT-4 translocation mediator Akt substrate of 160 kD (AS160) to promote the transport of glucose by GLUT4 [65,73]. This evidence concerns the gene AKT1 and cardiac hypertrophy.