Previous studies identified ROS as key factors that lead to oxidative stress injury in patients with hyperlipidemia, thereby damaging the myocardium.[18] ACSL1 exerts its function by directing the metabolic partitioning of FAs toward β‐oxidation in adipocytes, and its overexpression reduces FA oxidation through the PPARγ pathway.[19] Through bulk RNA‐seq, we revealed ACSL1 as a key mediator between hyperlipidemia and AMI. This evidence concerns the gene ACSL1 and hyperlipidemia.