MiR‐24 improved heart function and attenuated fibrosis in the infarct border zone of the heart 2 weeks after MI induced through intramyocardial injection of lentiviruses, which was related to the regulation of furin (a protease that controls latent TGFβ activation) and reduced TGFβ (a pathological mediator of fibrotic disease) secretion and Smad2/3 phosphorylation in cardiac fibroblasts 78. The gene discussed is TGFB1; the disease is myocardial infarction.