The mechanisms responsible for the attenuated catecholamine effects in heart failure (HF) are varied and include reduced adenylate cyclase activity and enhanced G-protein receptor kinase (GRK2) and intracellular protein phosphatase activity (PP1 and PP2A) which together lead to a decrease in cAMP-dependent signaling and impaired PKA-dependent target phosphorylation1,3,4. This evidence concerns the gene GRK2 and hydrops fetalis.