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). The gene discussed is PLCB3; the disease is hypertensive disorder.