TGFB1 and hydrops fetalis: Constituently, active forms of TGFβ, resistant to LAP inactivation, have been used in both large and small animal models to stimulate atrial and/or ventricular cardiac fibrosis resulting in HF, arrhythmias and reduced survival (Nakajima et al, 2000; Verheule et al, 2004; Accornero et al, 2015; Polejaeva et al, 2016).