Therefore, our results support the hypothesis that in heart failure the impaired myocardial oxidative metabolism in mitochondria, reflected by elevated myocardial citrate content (Figure 4A) and by a decreased mtDNA/nDNA (Figure 5D), is discerned to exert an impact on myocardial fuel oxidation (including BCAAs) leading to myocardial BCAAs retention (Figure 3A) and in consequence contributes to the heart dysfunction via BCAAs-dependent mTOR pathway activation (Karwi and Lopaschuk, 2023). This evidence concerns the gene MTOR and heart failure.