Remarkably, the restoration of the activity of this signaling complex after supplementation with leucine was accompanied by suppression of the anti-hypertrophic of MEF2C depletion, indicating that the defective activation of mTOR/S6K pathway is a critical component of the beneficial effects of MEF2C depletion in the cardiac phenotype of TAC mice. This evidence concerns the gene MTOR and persistent truncus arteriosus.