He et al. [53] found that the overexpression of miR-155 in acute myocardial infarction (AMI) induced cardiac fibrosis by directly targeting the Tp53inp1 gene and inhibiting its expression, while downregulated Tp53inp1 dramatically promoted the mRNA and protein expression levels of collagen I/III and increased the expression level of α-SMA in cardiac fibroblasts. Here, TP53INP1 is linked to myocardial infarction.