Upregulation of immunoproteasome catalytic subunit β5i leads to cardiac hypertrophy and heart failure (HF) by promoting ATG5 degradation (28), while Nrf2 ablation slows the progression of diabetic cardiomyopathy (DC) in cardiomyocyte-specific ATG5 KO mice (29). Here, ATG5 is linked to dyskeratosis congenita.