TREM1 and myocardial infarction: Nevertheless, TREM-1 pharmacological inhibition by the LR12 peptide (that impairs ligand/TREM-1 interaction and blocks the multimerization) or genetic invalidation reduces hyper-responsiveness and death during various experimental septic shock model (10–12), protects from cardiovascular dysfunction following myocardial infarction (13, 14), and prevents atherosclerosis (15, 16), and even cancer (17, 18).