NRF2 and its downstream target HO1 protect against myocardial hypertrophy, myocardial ischemia‐reperfusion, and other myocardial injuries.[49, 50, 51] As a stress‐inducible enzyme, HO1 catalyzes heme degradation to release free iron, carbon monoxide, and biliverdin from mammalian cells.[52] Overall, these data indicate that the SUMOylation of TEAD1 regulates CM enlargement and oxidative stress during cardiac hypertrophy. The gene discussed is TEAD1; the disease is cardiac hypertrophy.