Moreover, we provided direct evidence that IL-10 but not TGF-β1 or IL-35 played a protective role in exogenous Breg-mediated effects on MI, which was in accordance with the results of endogenous Bregs, as B cell-specific deletion of IL-10 worsened cardiac function and exacerbated myocardial injury after MI [49]. The gene discussed is IL10; the disease is myocardial infarction.