It has been long known that metabolic syndrome is associated with increased risk of CAD events.21 Both in vivo and in vitro studies have demonstrated that Metrnl could upregulate key transcription factors for adipocyte differentiation (PPARγ, C/EBPα) and lipid metabolism genes for lipid transport (FABP4, CD36), lipogenesis (ACC, FASN), lipolysis (Lipe, PNPLA), and lipid storage (Perilipin),13 indicating that Metrnl may mediate the link between metabolic disorder and CAD. Here, PLIN1 is linked to coronary artery disorder.