Several experimental studies have proven that the interaction between ST2L and IL-33 promotes cardioprotective effects, by limiting myocardial fibrosis, inhibiting cardiomyocyte hypertrophy, reducing apoptosis and upgrading the overall myocardial function via activation of myeloid differentiation primary response gene 88 (MyD88), interleukin-1 receptor-associated kinase (IRAK), extracellular signal-regulated kinase (ERK) and nuclear factor-κB (NF-κB) signaling pathways [44,49]. The gene discussed is IRAK1; the disease is Myocardial fibrosis.