DUSP6 and myocardial infarction: Here, by using CRISPR-induced Dusp6 mutant rats as reported previously19, as well as a newly established neutrophil-specific Dusp6-knockout mouse model, we found that Dusp6 deficiency improves cardiac repair and function by predominantly attenuating neutrophil activity at the acute inflammatory phase post-MI while having no effect on neutrophil development, differentiation, and injury-induced tissue infiltration.