ADRB1 and hydrops fetalis: By generating CM-specific TG mouse models for WT β1AR, one β1AR mutant lacking PKA phosphorylation sites and Gαs coupling (PKA–β1AR; β-arrestin-biased β1AR), and the other β1AR mutant lacking G protein-coupled receptor kinase [GRK] phosphorylation sites and β-arrestin coupling (GRK–β1AR; Gαs-biased β1AR), this study showed that GRK–β1AR TG had greater cardiac apoptosis and more severe HF than WT and two other lines of β1AR TG mice following chronic catecholamine treatment.