More importantly, knockdown NAP1L1 restored cardiac function post‐myocardial infarction (MI) and inhibited excessive deposition of ECM, and blocked the fibroblast‐to‐myofibroblast trans‐differentiation process, indicating that it can be a potential treatment target for myocardial fibrosis. This evidence concerns the gene NAP1L1 and myocardial infarction.