The previous study also showed that the elevated sympathetic activity in chronic heart failure cause enhanced GRK2-mediated cardiac β1-AR and β2-AR desensitization and β1-AR downregulation, the compensatory upregulation of β3-ARs, eventually leading to the progressive loss of the adrenergic, inotropic reserves of the heart, and the deterioration of cardiac function [11]. Here, ADRB2 is linked to congestive heart failure.