Stimulation of BM neutrophils with a supernatant from cardiac tissue after MI/R resulted in significantly greater STAT3 phosphorylation (Figure 5G) and upregulation of the pro-angiogenic genes Prok2 and Chil1 in Cd300a−/− neutrophils compared with WT neutrophils (Figure 5H), suggesting that CD300a suppresses the expression of pro-angiogenic and antifibrotic genes by inhibiting STAT3 activation in SiglecFlo neutrophils in cardiac tissue after MI/R. The gene discussed is CD300A; the disease is myocardial infarction.