Abnormal MCU or NCLX causes mCa2+ shuttling system disorder, but research showed that an MCU knockout yielded a relatively mild phenotype, and a conditional knockout of NCLX led to rapid fatal heart failure [28], which suggests that NCLX-mediated efflux is necessary to maintain homeostatic mCa2+ levels in cardiomyocytes and for survival. This evidence concerns the gene MCU and heart failure.