Therefore, colchicine directly inhibits neutrophil chemotaxis and activity in response to vascular injury, indirectly reduces the production of active interleukin IL-1β via inhibitory effects on the inflammasome,5 and reduces neutrophil–platelet aggregates, which may accumulate in the microvascular beds, for example, during acute myocardial infarction (MI) or contributing to myocardial injury after percutaneous coronary intervention.9 The gene discussed is IL1B; the disease is myocardial infarction.