A few years later, Tao et al. found that miR-433 could induce TGF-β1 expression level by inhibiting AZIN1 expression level [70], which is a regulator of polyamine synthesis with an undefined relationship with TGF-β1 Furthermore, after MI, the miR-21 and miR-328 decrease TGFβRIII expression level, which could directly neutralize TGF-β1 and contribute to excessive ECM production and cardiac fibrosis [57,66]. This evidence concerns the gene TGFB1 and myocardial infarction.