ACS leads to compromised diastolic function and myocardial ischemia,17 when cardiomyocytes and cardiac fibroblasts are subjected to injury and mechanical stress, a significant increase of release in ST2L and ST2, which acts as a decoy receptor for IL‐33 and can competitively inhibit the binding of IL‐33 to ST2L, thus limiting the protective effect of IL‐33 on the heart.18 The gene discussed is IL1RL1; the disease is myocardial ischemia.