CTBP1 and hydrops fetalis: Genetic deletion of β-arrestin1 in the heart leads to many effective therapeutic consequences in HF, which include improvements in inotropic reserves along with cardiac βARs, enhanced severe adverse cardiac remodeling, and the elevated longevity of β-arrestin-1-knockout mice (β-arrestin1 KO) with post-myocardial infarction (MI) HF [52,53].