PlGF overexpression in cardiac tissues was also found to be associated with increased endothelial-derived NO release which promoted cardiomyocyte hypertrophy by activating the Akt/mTORC1 pathway, whereas conditional cardiac-specific PlGF expression in eNOS knockout mice failed to induce myocardial hypertrophy (111). The gene discussed is PGF; the disease is cardiac hypertrophy.