Further, miR-29a, which is upregulated early in the process of healthy cardiac progenitor cell differentiation, was determined to target and downregulate DNMT3A expression (Figure 5), suggesting that overexpression of miR-29a is a potential therapeutic modality to regulate the DNMT3A-Wnt axis and promote cardiomyocyte regeneration after MI [86]. This evidence concerns the gene DNMT3A and myocardial infarction.