In decompensated HF, autophagy and mitophagy were suppressed, coinciding with down‐regulated mitochondrial translocation of DNM1L/Drp1.6 MCU silencing could promote DNM1L/Drp1‐mediated mitochondrial fission and apoptotic cell clearance, avoiding the pathologic accumulation of metabolic products in vivo.5 Based on these thought‐provoking studies, we reckon that insufficiency of autophagy and mitophagy was underlying the initiation and maintenance of HF, while CRT could change the expression of MCU and DNM1L/Drp1 and partly restore cardiac autophagy. The gene discussed is DNM1L; the disease is hydrops fetalis.