Monocyte-derived macrophage subsets (CCR2+MHC-IIhigh, CCR2+MHC-IIlow and CCR2+Ly6Chigh) are preferentially recruited to sites of injury, where they enhance inflammation by promoting further monocyte and neutrophil recruitment and cause cardiomyocyte hypertrophy, interstitial fibrosis and adverse cardiac remodeling resulting in poor outcome, e.g. after myocardial infarction (Lavine et al., 2014; Li et al., 2016; Lorchner et al., 2018). This evidence concerns the gene CCR2 and myocardial infarction.