Ting Liu et al. (59) found that overexpressed MCU during cardiac decompensation may reverse the course of heart failure, improve the contractile response of cardiomyocytes, and suppress HF-related arrhythmias by enhancing mitochondrial Ca2+ accumulation, reducing mitochondrial oxidative stress, and mitigating SR Ca2+ leakage. The gene discussed is MCU; the disease is hydrops fetalis.