Although activation of the α1A adrenoceptor can be a crucial factor in the development of MI, the relationship between ILK and MI, particularly the ability of an α1A adrenoceptor blocker to attenuate MI via modulation of the ILK-related TGF-β/Smad pathway through the fibrotic pathway, still needs further clarification. The gene discussed is ILK; the disease is myocardial infarction.