Indeed, T cells in patients with acute coronary syndromes (ACS) are skewed toward the production of interferon (IFN)-γ, a potent monocyte activator largely derived from a distinct subset of CD4+ T cells [6,7] that, in contrast to classic CD4+ helper T cells, lacks the costimulatory molecule CD28 [8]. The gene discussed is CD4; the disease is acute coronary syndrome.