Our previous studies have demonstrated that cardiac pathological stress triggers the expression of Flt3 in cardiomyocytes, and Flt3 activation with its specific ligand (FL) remarkably reversed Angiotensin II or isoprenaline (ISO)-induced cardiac hypertrophy and cardiac adverse remodeling through AMPK/mTORC1/FoxO3a or SIRT1/p53 signaling [13,14]. The gene discussed is AGT; the disease is cardiac hypertrophy.