Atorvastatin is an orally active HMG-CoA reductase inhibitor, has the ability to effectively decrease blood lipids. Atorvastatin inhibits human SV-SMC proliferation and invasion with IC₅₀s of 0.39 μM and 2.39 μM, respectively^[1][2][3]. In Vitro: Atorvastatin treatment decreases apoptosis of myocardial cells by down-regulating GRP78, caspase-12 and CHOP expression in myocardial cells after myocardial infarction, and the endoplasmic reticulum (ER) stress is activated in response to heart failure and angiotensin II (Ang II) stimulation^[4]. In Vivo: Atorvastatin (20-30 mg/kg; oral gavage; once a day; for 28 days; ApoE^−/− mice) treatment significantly reduces endoplasmic reticulum (ER) stress signaling proteins, the number of apoptotic cells, and the activation of Caspase12 and Bax in the Ang II-induced ApoE-/- mice. Proinflammatory cytokines such as IL-6, IL-8, IL-1β are all remarkably inhibited after Atorvastatin treatment^[5].