β-arrestin binding to β1ARs results into the uncoupling of Gs from β2ARs, which together with the GRK2-phosphorylation of β2ARs results into enhanced Gi-biased signaling downstream β2ARs, the activation of CaMKII pathways and the further uncoupling of Gs from β1ARs.30 In accordance with the Gi-biased signaling in HF, there are some promising data of a combinational therapy for HF employing β1ARs selective blockers and a Gs-biased β2ARs agonist. The gene discussed is GRK2; the disease is hydrops fetalis.