NFKB1 and endothelial dysfunction: IH, the hallmark of OSAHS, induces recurrent surges of reactive oxygen species that activate NF‐κB, HIF‐1α, and other redox‐sensitive pathways, driving systemic oxidative stress, endothelial dysfunction, and DNA damage, all of which create a microenvironment conducive to tumor initiation and progression [54].