However, when the heart is subjected to damage or mechanical stress, cardiomyocytes and cardiac fibroblasts secrete sST2, which, competing with ST2L for the IL-33 binding site, antagonizes the cardioprotective effect, contributing to myocardial fibrosis and ventricular remodeling [12,19,20]. The gene discussed is IL1RL1; the disease is Myocardial fibrosis.