Dusp6 deficiency in neutrophils upregulates pERK and DUSP1/DUSP16, thus attenuating p-p38, neutrophil respiratory burst and degranulation, and finally resulting in reduced neutrophil-mediated cardiac damage after MI while Dusp6 has minimal effect on other immune cell subsets in post-MI cardiac remodeling (Supplementary Fig. 21). This evidence concerns the gene DUSP16 and myocardial infarction.