In our study, the infiltration of Ccr2+ monocytes/macrophages in the hearts of Klf9–/– mice post-MI was reduced (Figure 4B and Figure 7, C and D), which could lead to delayed wound healing because necrotic tissue was not cleared in time; thus, granulation tissue and collagen matrix were slowly formed. The gene discussed is KLF9; the disease is myocardial infarction.