Treatment with the β-blocker carvedilol or GRK2 inhibitors attenuates insulin-induced phosphorylation of extracellular regulated protein kinases and phosphodiesterase 4D (PDE4D) induction in 2-adrenergic receptor (β2AR) or β-arrestin2 knockout mice fed with HFD, thereby reducing systolic dysfunction in DCM [60]. The gene discussed is INS; the disease is familial dilated cardiomyopathy.