Moreover, the ER stress inhibitors, 4-phenyl butyrate (PBA) or tauroursodeoxycholic acid (TUDCA) have proved effective in reducing blood pressure and improving vascular reactivity in angiotensin II (Ang II)- or tunicamycin-infused mice and spontaneously hypertensive rats (SHRs), indicating that ER stress may have been a cause of endothelial dysfunction and thus a key factor for these cardiovascular disorders5,12. The gene discussed is AGT; the disease is Endoplasmic Reticulum Stress.