For example, platelet activation and platelet‐monocyte aggregates in acute coronary syndrome are used as an early hallmark for acute myocardial infarction.12 Furthermore, platelet‐monocyte aggregates after myocardial infarction are more sensitive markers of platelet activation than P‐selectin.13 However, it is unclear whether these interactions are a cause, an active participant, or merely an epiphenomenon of the inflammatory response. This evidence concerns the gene SELP and myocardial infarction.