However, the findings are consistent with ex vivo demonstration of an increasing number of CXCR4+ cells within the vascular wall as atherosclerotic lesions progress, and they are also consistent with prior intravascular ultrasound observations of several high-risk plaque ruptures at sites other than the culprit lesion in acute coronary syndromes [33, 34]. The gene discussed is CXCR4; the disease is acute coronary syndrome.