The decreased presence of resident and/or blood circulating BDNF and NGF was described in metabolic syndrome, human coronary atherosclerosis, and acute coronary syndromes [3,4,5,6,7,9,10], suggestive of (i) a key function played by BDNF and NGF in the pathogenetic processes and (ii) a potential therapeutic action of TrkBBDNF and TrkANGF receptor agonists in CMD. The gene discussed is BDNF; the disease is acute coronary syndrome.