Clinical studies have demonstrated that prophylactic administration of Dex significantly reduces the incidence of postoperative delirium following surgical procedures.[16] Extensive animal and experimental research has further elucidated the neuroprotective mechanisms of Dex, suggesting that it may attenuate neuronal apoptosis induced by ischemia-reperfusion (I/R) injury through inhibition of the HIF-1α pathway, thereby ameliorating cerebral I/R injury.[16,17]. The gene discussed is HIF1A; the disease is delirium.