Furthermore, Nur77 agonist and AMPK siRNA or knockout abolished the beneficial effects of FGF1ΔHBS on HG with/without PA-induced cardiomyocyte dysfunction (Fig. 6) or DCM in vivo (Fig. 7), which indicates an AMPK activation/Nur77 suppression/mitochondrial homeostasis pathway under FGF1ΔHBS treatment. The gene discussed is PRKAA2; the disease is familial dilated cardiomyopathy.