SOAT1 and coronary artery disorder: (b) miR‐26a inhibited the apoptosis of endothelial cells through regulating janus kinase (JAK)/signal transducers and activators of transcription (STAT) and mitogen‐activated protein kinase (MAPK)/vascular endothelial growth factor (VEGF) pathways, which further prevented endothelium from being damage, thus led to reduced risk of CHD.18, 19