Our recent studies address this conundrum by showing that oxidative stress (a stimulus that contributes to the pathogenesis of heart failure and various other cardiomyopathic syndromes) decreases β1AR expression and isoproterenol responsiveness in cardiomyocytes; oxidative stress does not lead to changes in the expression of the β2AR subtype (20). The gene discussed is ADRB1; the disease is heart failure.