GRK2 and systolic heart failure: Accumulating evidence has shown that chronic stimulation of cardiac β-adrenoceptors activation leads to receptor phosphorylation via GPCR kinases i.e. βARK1 (desensitization), subsequent internalization of desensitized receptors via β-arrestin (downregulation), a loss of β-adrenoceptor mediated signalling, and finally the development of systolic heart failure (reviewed by [28]).