HNMT and myocardial infarction: DYRK1A (bispecific tyrosine regulatory kinase 1A), which has the ability to regulate blood glucose, has been found to phosphorylate HAT KAT6A and HMT WDR82 in myocardial infarction, thereby inhibiting histone acetylation and methylation levels of cell cycle-related genes and hindering post-myocardial infarction cardiac repair [29–31].