In addition, in vivo inhibition of GRK2 only in cardiomyocytes, at or after birth, was able to ameliorate cardiac contractility and reverse adverse ventricular remodeling through improved β-AR signaling in an ischemic model of HF, confirming the specific pathological role of GRK2 in cardiomyocytes (Raake et al., 2008). The gene discussed is ADRB2; the disease is hydrops fetalis.