EPAS1 and gastroesophageal reflux disease: In nicotine‐induced GERD, HIF‐2α in esophageal epithelial cells activated the NF‐κB signaling pathway and stimulated the production of proinflammatory cytokines [34]; in hypoxia‐induced OA, HIF‐2α mediated primary cilia loss in primary chondrocytes of mice under hypoxic conditions via the HIF‐2α/AURKA/NEDD9 pathway, which facilitated the development of OA [62].