A dose-dependent increase in the methylation of the Treg-specific demethylated region in FOXP3 was observed in cultures of peripheral blood mononuclear cells in patients with acute coronary syndromes [36], suggesting that epigenetic suppression of FOXP3 might lead to down-regulation of Treg cells, and in turn increase the risk of atherosclerosis. The gene discussed is FOXP3; the disease is acute coronary syndrome.