In aged Atrogin-1 knockout mouse hearts, CHMP2B turnover is diminished leading to its intracellular accumulation/aggregation, impairment of autophagy and finally proteotoxic ultrastructural alterations in cardiomyocytes and heart failure [14], highlighting the importance of orchestrated protein degradation in muscle cells to prevent heart and skeletal muscle damage. This evidence concerns the gene CHMP2B and heart failure.