Consistent with the findings from previous studies, the immunohistochemistry and immunofluorescence findings from the present study in acutely aspirated coronary thrombi and autopsy specimens from patients with STEMI suggests that the increase in plasma S100A12 in STEMI derives from its acute release from CD68+ macrophages in ruptured plaques, a mechanism quite different than the elevation of biomarkers derived from myocardial necrosis such as CK-MB and hscTnT (16). The gene discussed is S100A12; the disease is necrosis.