Several reports have stressed the relevance of metabolic activity as a crucial nexus between cardiac and immune cells, as metabolic disorders can give rise to the accumulation of abnormal levels of metabolites that can impact immune cell functionality.[10] Metabolic dysregulation emerged early in the pathogenesis of MI and coincided with extensive pro‐inflammatory CCR2+ monocyte/macrophage infiltration in the present study. This evidence concerns the gene CCR2 and myocardial infarction.