SNP-induced reduction of miR-590 levels could lead to de-repression of TGFβRII (target of miR-590-5p[23]) and Acvr2a (target of miR-590-5p/3p), receptors involved in TGF-β and Activin A signaling, respectively, which in turn could influence cardiac hypertrophy and fibrosis (cardiac remodeling) and thus, clinical outcomes in the setting of cardiomyopathies and following myocardial infarction [18]. This evidence concerns the gene TGFB1 and cardiac hypertrophy.