Additionally, recent preclinical studies have identified the indispensable role of BRD4 in mouse hearts and highlighted the therapeutic benefits of BET BD inhibition in various types of heart disease, including myocardial infarction (MI) or transverse aortic constriction (TAC)-induced heart failure (HF), gene mutation-induced dilated cardiomyopathy (DCM), and dyskeratosis congenital (DC) [29,30,31]. Here, BRD4 is linked to hydrops fetalis.