Interestingly, an additional study utilizing a rabbit model, also showed that reintroduction of caveolin-3 was able to normalizes β-adrenergic-induced contractile responses in HF myocytes, while also showing that in HF β2-induced signaling gains access to myofilament which may contribute to abnormal PKA phosphorylation of troponin I and contractile dysfunction (Barbagallo et al., 2016). The gene discussed is CAV3; the disease is hydrops fetalis.