Furthermore, Fan et al. [50] demonstrated that elevated lactate levels post-myocardial infarction induce Snail1 lactylation via the TGF-β/Smad2 pathway, promoting endothelial-to-mesenchymal transition (EndoMT), thereby exacerbating cardiac fibrosis and functional impairment, unveiling a previously unrecognized role of lactate in exacerbating adverse cardiac outcomes. The gene discussed is SNAI1; the disease is myocardial infarction.