Accordingly, if Cav3 is disrupted in healthy cardiomyocytes, stimulation of β2ARs results into a similar effect to the one observed in HF.25 Even more importantly, reintroduction of Cav3 in failing rabbit cardiomyocytes can normalize the β2AR signal and restore the contractile response to adrenergic stimulation.59 Co-immunostaining of control cardiomyocytes confirm that the total percentage of Cav3 that is co-stained with β2AR is higher (47%) than with β1AR (39%; Figure S5B). The gene discussed is CAV3; the disease is hydrops fetalis.