Efficient phagocytosis by microglia requires dynamic cytoskeletal reorganization, a process heavily dependent on adenosine triphosphatase (ATP).[16] Prior studies have demonstrated that MRP14 induces mitochondrial dysfunction through TLR4 after myocardial infarction.[17] Consistently, KEGG pathway analysis of cluster 1 signature genes identified enrichment in pathways related to the tricarboxylic acid cycle, respiratory electron transport, and ATP synthesis (Figure 4F). This evidence concerns the gene S100A9 and myocardial infarction.