Conversely, PKM2 expression has been found to be upregulated in stressed hearts where it has contributed to HF [40], while inhibition of the PKM2/β-catenin axis in post-MI mice reduced infarct size, increased the percentage of proliferative cardiomyocytes, improved mitochondrial function, and enhanced angiogenesis, which was attributed to the activation of target genes associated with cell proliferation [41]. This evidence concerns the gene PKM and myocardial infarction.