Particularly, β-arrestin 1 knockout (KO) mice have shown improved cardiac function (enhanced EF and inotropic reserve) in a model of ischemic HF: the underlying mechanisms are, on one side, improved cardiac β-AR signaling and function due to cardiac β-arrestin 1 deletion, and on the other, decreased circulating levels of CAs and aldosterone due to adrenal β-arrestin 1 absence (Lymperopoulos et al., 2011; Bathgate-Siryk et al., 2014). This evidence concerns the gene ADRB2 and hydrops fetalis.