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. Here, GZMK is linked to hydrops fetalis.