In conclusion, this preclinical trial suggests that the use of hCD16+ Ms to treat acute MI is feasible and safe and it is associated with reduced LV scar size, increased tissue levels of neo-angiogenesis and myofibroblasts and reduced pro-fibrotic TGF-β at 30 days despite immunosuppression. Here, TGFB1 is linked to myocardial infarction.