In acute myocardial infarction (AMI), HOTTIP knockdown markedly promoted cardiomyocyte growth and inhibited cardiomyocyte apoptosis in vitro, and miR-92a-2 overexpression could significantly enhance the protective effect of HOTTIP knockdown against AMI through partially inhibiting c-Met expression 49. This evidence concerns the gene HOTTIP and acute myocardial infarction.