Following augmented cardiac loads (augmented pressure and biomechanical stress, and tension of the muscular structures) associated with acute myocardial infarction (AMI) or progressive heart failure (HF), cardiomyocytes, endothelial cells and cardiac fibroblasts increase the expression and release of both ST2 forms and IL-33 [4,28,29]. This evidence concerns the gene IL1RL1 and hydrops fetalis.