Although treatment and prevention of MI have achieved great progress in the past few years, patients with MI still face a modest risk of heart failure due to the failed compensation of apoptotic cardiomyocytes.8 The whole‐genome transcriptome analysis has showed that many cardiac‐specific lncRNAs involve in many unique functions and regulations related to myocardial remodelling, myocardial regeneration and heart function.34 This study was conducted to investigate the role of mouse ATP2B1‐AS1 in MI based on its related bioinformatics information. This evidence concerns the gene ATP2B1 and heart failure.