We also investigated whether sustained mTORC1 activation exhausts the capacity of the endoplasmic reticulum (ER) to fold proteins correctly, induces ER stress,10 and leads to contractile dysfunction in both rodent and human models of heart failure.11 The results suggest that dysregulated glucose metabolism mediates load‐induced contractile dysfunction by activating mTOR and inducing ER stress. Here, MTOR is linked to heart failure.