To the Editor, Atherosclerosis is the leading cause of death in the united states and accounts for more than half of all mortalities in developed societies. The current attitude toward the pathophysiology of atherosclerosis considers inflammation as a major contributor that mediates nearly all phases of this disease. C-reactive protein (CRP) is an acute-phase protein which has long been regarded as a well-known and sensitive biomarker of systemic inflammation. There is a considerable body of evidence indicating CRP as a powerful cardiovascular risk predictor [1]. Hence, its measurement has been included in the guidelines issued by the American Heart Association/Centers for Disease Control and Prevention (AHA/CDC), for cardiovascular risk assessment [2]. Aside from its role as a risk marker, there are recent reports on the involvement of CRP in atherogenesis and thereby its potential role as a cardiovascular risk factor [3]. Based on these findings, CRP reduction may represent a novel therapeutic approach against cardiovascular diseases. Nevertheless, there has been no drug designed specifically for CRP lowering [4]. Several studies have reported that CRP binds with high affinity to phosphatidylcholine (PC) in a calcium dependent manner [5, 6]. In a similar way, CRP can bind and aggregate low-density lipoprotein (LDL) particles [7, 8], in particular oxidized LDL (ox-LDL) [9]. This clustering of LDL by CRP enhances the uptake of LDL/CRP complexes by macrophages and finally leads to the formation of foam cells [7, 8], which are a typical characteristic of atherosclerotic plaques. Therefore, reduction of serum CRP levels may theoretically blunt the process of atherogenesis via reducing the aggregation of ox-LDL and subsequent formation of foam cells. Herewith I would like to propose a simple strategy, based on nanoliposomes, for the purpose of serum CRP reduction. Nanoliposomes are known to be rapidly and effectively uptaken from the bloodstream by macrophages. This uptake mainly occurs by kupffer cells which are specialized and resident macrophages of the hepatic tissue. Biocompatible and biodegradable nanoliposomes containing PC as their major phospholipid constituents could be easily synthesized [10]. Serum CRP is expected to bind these PC-rich nanoliposomes. Afterwards, these complexes will be effectively removed from circulation via the action of the reticuloendothelial system (mainly kupffer cells). These complexes will then be directed to lysosomes [11], where CRP will be digested by acid hydrolases into its constituent amino acids. Since thousands of PC molecules are present in each nanoliposome, a high efficacy would be anticipated for such a system. The binding of synthetic PC containing nanoparticles to CRP has been recently reported for PCcoated gold nanoparticles [12]. However, liposomes appear as a better option for therapeutic purposes owing to their membrane structure (which permits abundant inclusion of PC), safety, biocompatibility and biodegradation. This simple and inexpensive nanoliposomal formulation may represent a potential therapy for rapid CRP reduction and preventing its interaction with ox-LDL. Moreover, regarding the pro-inflammatory activities of CRP [13], such a strategy may also work for multiple inflammatory diseases. A. Sahebkar (*) Cardiovascular Research Center, Avicenna Research Institute, Mashhad University of Medical Sciences (MUMS), P. O. Box: 91775-1365, Mashhad, Iran e-mail: sahebkarah811@mums.ac.ir