Critically, this pathway is implicated in hypertensive vascular dysfunction, where metabolites such as trimethylamine N‐oxide (TMAO) activate the PERK‐eIF2α‐ATF4‐CHOP axis, exacerbating endothelial dysfunction and compromising vascular integrity—effects that are mitigated by PERK downregulation [39]. This evidence concerns the gene EIF2AK3 and endothelial dysfunction.