TMAO could also promote Ang II–induced vasoconstriction via the PERK/ROS/CaMKII/PLCβ3 (protein kinase r-like endoplasmic reticulum kinase (PERK), reactive oxygen species (ROS), calmodulin-dependent protein kinase ΙΙ (CaMKΙΙ), phospholipase c β3 (PLCβ3) axis, thereby facilitating Ang II–induced hypertension (126). This evidence concerns the gene EIF2AK3 and hypertensive disorder.