In the HIV-uninfected population, statin therapy produced significant and rapid dose-dependent reductions in FDG update that were reflective of changes in atherosclerotic plaque inflammation. In addition, lipoprotein apheresis resulted in significant reduction of arterial inflammation. Recently, addition of evolocumab was found to result in a greater decrease in percent atheroma volume using intravascular ultrasound. All of these studies which were performed in the non-HIV population provide a strong scientific rationale for studying the role of PCSK9 inhibition in HIV. Namely, given the strong association between HIV, noncalcified plaque, and arterial inflammation, PCSK9 therapy may play a unique role in reducing HIV-associated atherosclerosis, Alirocumab (Sar236553/REG 727) is a fully humanized monoclonal antibody against the proprotein convertase subtilisin kexin type 9 (PCSK9) enzyme responsible for the degradation of the low-density lipoprotein receptor (LDLR), and is developed by Regeneron Pharmaceuticals/Sanofi. In a randomized trial of 2341 patients with heterozygous familiar hypercholesterolemia or with established coronary heart disease or a CHD risk equivalent with LDL levels≥70mg/dL and were receiving treatment with statins at the maximum tolerated dose with or without other lipid-lowering therapy. Patients were randomly assigned to a 2:1 ratio to receive alirocumab 150mg or placebo every 2 weeks for 78 weeks. At week 24 the difference between the alirocumab and placebo groups from baseline to calculated LDL was -62 percentage points. The alirocumab group had higher rates of injection site reactions, myalgia, neurocognitive events and ophthalmologic events. The rate of major adverse cardiovascular events was lower in the alirocumab group as compared to placebo in a post hoc analysis (p=0.02).