These results are comparable with those found in CCR1-deficient mice, or after anti-CCL5 mAb treatment, which showed that the initial inhibition of CCL5 during early MI is cardioprotective owing to its anti-inflammatory effects [8,9], reducing both infarct size and post-infarction heart failure in mouse model of chronic cardiac ischaemia [29]. This evidence concerns the gene CCL5 and myocardial infarction.