Our finding that CD32-positive circulating monocytes are more abundant in patients who develop AHR are in line with those in other reports that suggested that upregulated CRP levels may promote the differentiation of human CD32 monocytes towards an M1 proinflammatory phenotype [33,34], thereby amplifying myocardial damage and contributing to development of heart failure after an initial non-myocardial infarction ACS. The gene discussed is CRP; the disease is heart failure.