Of these, cMo and iMo have been shown to be directly related to cardiac dysfunction.[56–60] The literature reports an increased frequency of iMo (iMo_HLADR + CXCR3 + CD206+) in patients with cardiovascular disease and that upregulation of iMo is associated with plaque rupture.[61] Several studies have shown that natural killer T cells promote atherosclerosis formation and facilitate plaque rupture.[62–65] In addition to the previously mentioned CD8 + Tregs, CD8 + T cells are involved in the formation of atherosclerosis and the development of MI in a perpetrator fashion. The gene discussed is MOS; the disease is myocardial infarction.