Consistent with our earlier observations in Cd300a−/− mice (Figure 1), treatment with the anti-CD300a mAb reduced the plasma cTnI level, increased angiogenesis, improved LVFS and LVEF, and reduced fibrosis compared with control antibody injection after MI/R (Figure 6, A–D). The gene discussed is TNNI3; the disease is myocardial infarction.