Cardiac BCAA catabolism is described to be deregulated also in myocardial infarction (MI)-operated mice, and this effect contributes to post-MI HF and remodeling by enhancing the mammalian target of rapamycin (mTOR) signaling, a modulator of various anabolic (e.g., protein synthesis) and catabolic (e.g., autophagy) pathways [65]. This evidence concerns the gene MTOR and hydrops fetalis.