Although Sanada et al. concluded such part of their experiment only outlining the importance of deletion of ST2 in the general outcome of cardiac structure undergone angiotensin II action, one more idea could be represented by the possible role of ST2 as therapeutic target: IL-33 external administration in patients suffering from cardiac diseases could enhance ST2L activation and its own biochemical intracellular pathway in order to prevent or at least reduce the worsening of the clinical and structural condition of the heart. Here, IL1RL1 is linked to heart disorder.