Lower GAS5 levels in the hypertensive group could be explained by the fact that GAS5 was discovered to be primarily expressed in endothelial cells/vascular smooth muscle cells (ECs/VSMCs) and its expression was significantly downregulated in hypertension; additionally, GAS5 knockdown exacerbated hypertension-induced microvascular dysfunction by influencing several pathways such as EC multiplication, VSMC phenotypic transformation, and EC-VSMC interaction via β -catenin signaling [11]. This evidence concerns the gene GAS5 and hypertensive disorder.