As co-factors of GRKs in cardiomyocyte β1AR desensitization and downregulation, βarrs contribute to the diminished inotropic and adrenergic reserves of the failing heart and their inhibition should theoretically be beneficial in acute HF, as it would enhance the Gαs-AC-PKA-mediated pro-contractile signaling of cardiac βARs, which increases cardiac contractility [3]. The gene discussed is ADRB1; the disease is hydrops fetalis.