Histone lactylation in monocytes promotes early activation of reparative gene expression, crucial for immune homeostasis and cardiac repair post-myocardial infarction, by regulating anti-inflammatory and pro-angiogenic activities.541 Inhibition of DYRK1A via histone modification, promotes cardiomyocyte cell cycle activation and cardiac repair after MI.542 Also, nucleophosmin1 recruits histone demethylase KDM5b to the TSC1 promoter, reducing H3K4me3 and TSC1 expression. The gene discussed is KDM5B; the disease is myocardial infarction.