Given that PRKAG2 is the AMPK regulatory subunit, we hypothesize that PRKAG2-AS regulates cardiomyopathy through the transcriptional control of PRKAG2. As a result, our study found that PRKAG2-AS can act as a regulatory element to modulate AMPK activity by regulating the transcription of the PRKAG2 gene and participate in regulating the occurrence of cardiovascular disease. This evidence concerns the gene PRKAG2 and cardiovascular disorder.