Lipsky et al. (2008) found that persistent activation of β-adrenergic receptors induced dysfunction of L-type Ca2+ channels via internalization of cardiac Cav1.2 channel complexes. Moreover, the β-adrenergic receptor signaling pathway is abnormally regulated. L-type Ca2+ channels can be modulated through activation of β-adrenergic receptors (β-Ars), which leads to an increase in ICa-L density as a result of phosphorylation by cAMP-dependent protein kinase A. Sustained β-AR activation in HF induces desensitization of β-Ars and leads to a reduction of ICa-L density. The gene discussed is CTBP1; the disease is hydrops fetalis.