On the one hand, Ludger Hauck et al. claimed that Pkm2 can directly interact with β-connexin (Ctnnb1) in the cytoplasm of cardiomyocytes (CM), inhibit the phosphorylation of Ctnnb1 via Akt at Ser552 and Try333, prevent Ctnnb1 from translocating to the nucleus, and then inhibit the transcription of proliferation-associated target genes (such as Myc and Cyclin D1) transcription, which adversely affects cardiac repair after myocardial infarction [137]. The gene discussed is CTNNB1; the disease is myocardial infarction.