The ablation of periostin-expressing cardiac fibroblasts with diphtheria toxin in a mouse MI model also reduced excess fibrosis but did not affect the scar thickness or the integrity of the infarct heart, and it increased the proportion and size of cardiomyocytes in the infarct area and improved cardiac function post-MI (Kaur et al., 2016). This evidence concerns the gene POSTN and myocardial infarction.