The main function of adrenal GRK2 in sympathetic overactivity and consequent progression of HF became more evident when we tried to contrast GRK2 increase by direct adrenal injection of its inhibitor β ARKct in HF rats (this peptide is the C-terminal part of GRK2 that doesn't contain the phosphorylation portion but competes with GRK2 for G-proteins βγ subunits binding). The gene discussed is GRK2; the disease is hydrops fetalis.