GNAI1 and hydrops fetalis: Chronic sympathetic activation is detrimental for the heart and sustained overexpression of β1AR triggers myocyte apoptosis and hypertrophy leading to HF.8 Sustained β-adrenergic stimulation leads to reduced expression and/or compensatory desensitization of βARs to catecholamines, both features of the functionally impaired heart.9 Increased expression of Gi—particularly of the α-2 subunit (Giα-2)—is also observed in HF, where enhanced β2AR-Gi coupling triggers diminished basal contractility following receptor activation.