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). The gene discussed is TREM1; the disease is atherosclerosis.