Previous studies found that QL improved cardiac metabolism and mitochondrial function in heart failure induced by pressure overload, while QL also enhanced the metabolism of H9C2 cardiomyocytes by regulating peroxisome proliferator-activated receptor gamma (PPARγ) coactivator-1α (PGC-1α) expression [18, 19]. The gene discussed is PPARGC1A; the disease is heart failure.