Finally, it is worth noting that the fact that Gαi is elevated in the failing human heart means that interventions such as GRK2 inhibition, aimed at increasing βAR-elicited Gs protein signaling that is depressed in human HF due to elevated GRK2-dependent desensitization [101,102], would probably be ineffective at sufficiently improving cAMP levels and, consequently, cardiac function. Here, GRK2 is linked to hydrops fetalis.