In this scenario, the persistent activation of MTORC1 lowers the capacity of cardiomyocytes to sustain pressure overload‐induced stress, as testified to by the fact that mice bearing knock‐in mutation in the MTORC1 inhibitor Tsc2 (TSC complex subunit 2) develop heart disease (Taneike et al, 2016), while succumbing to pressure overload (Ranek et al, 2019). Here, TSC2 is linked to heart disorder.