Based on multiple previous observations and the assumed role of sST2 in the fibrotic response to myocardial tissue injury, it is important to highlight that the release of sST2 by cardiac fibroblasts and cardiomyocytes is closely related to two profibrotic conditions, very common in HF with reduced ejection fraction (HFrEF): biomechanical strain and elevated Ang II [49,52]. This evidence concerns the gene AGT and hydrops fetalis.