When GRK2 ability to suppress β-adrenergic signaling is reduced by overexpression of GRK2 C-terminus that outcompetes endogenous full-length kinase for the G protein βγ-subunit, which targets GRK2 to the plasma membrane where β-adrenergic receptors reside, heart failure is alleviated (Tevaearai et al., 2001). The gene discussed is GRK2; the disease is heart failure.