Taken together, although other cell types in addition to Cd300a−/− BM neutrophils were also involved in the effect of STAT3i in vivo, these results suggest that pro-angiogenic genes are induced via the G-CSF/STAT3 axis, which is inhibited by CD300a in SiglecFlo neutrophils and attenuates cardiac dysfunction after MI/R. This evidence concerns the gene STAT3 and myocardial infarction.