MCU was believed to take an active part in mitochondrial pathophysiology.2 Zaglia et al reported MCU was elevated in angiotensin‐II‐induced cardiac hypertrophy, while microRNA‐1 could inhibit MCU's expression and alleviate cardiac dysfunction.35 MCU knockout could promote autophagy in vivo or in vitro,8, 36 and our previous study verified up‐regulation of autophagy and mitophagy after MCU knockdown in H9c2 cells originating from mouse cardiomyocytes.9 DNM1L/Drp1 was closely related to mitochondrial fission and mitophagy. The gene discussed is DNM1L; the disease is cardiac hypertrophy.