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]. The gene discussed is IL33; the disease is hydrops fetalis.