CFs are the principle cell type responsible for cardiac fibrosis; they secrete a variety of MMPs to promote ECM degradation, thus increasing CF migration, fibrosis, and negative cardiac remodeling.[37] Increased MMP2 and MMP9 expression contributes to CF migration in vitro.[22, 38] Consistently, we found that NKRF significantly inhibited the increase in inflammatory cytokine‐induced expression and activities of MMP2 and MMP9. Here, NKRF is linked to cystic fibrosis.