showed that β-adrenergic signaling in vitro and pressure overload in mice increased the level of S573-phosphorylated B56δ, a mechanism that would be consistent with neurohormonal activation in HFrEF and the beneficial effects of β-blockade in ischemic and non-ischemic DCM.27 Here, PPP2R5D is linked to familial dilated cardiomyopathy.