Others have shown that, functionally, CCR2-receptor deficiency results in a diminished ejection fraction after myocardial infarction during long-term recovery compared to wild-type, CX3CR1- and MCP-1 KO mice24 and we found that hyperenhancement and expansion index were greatest in CCR2-KO mice 30 days post-MI. This evidence concerns the gene CX3CR1 and myocardial infarction.