**1. Introduction**

Initial understandings of high-density lipoprotein (HDL) came from the epidemiological studies, which consistently showed that a low HDL cholesterol (HDL-C) level is regarded as an independent risk for the development of cardiovascular disease (CVD) [1, 2]. Inversely, elevated HDL-C concentration in plasma is correlated with reduced CVD risk [3]. Therefore, lots of strategies for raising HDL-C were considered to be the suitable targets for CVD prevention and treatment [4, 5]. Deficiency and inhibition of cholesterol ester transfer protein (CETP) increase plasma HDL-C levels; however, they do not necessarily reduce CVD risk as expected, which suggest that the compositions and functions of HDL are more complicated than we supposed before [6]. Besides reverse cholesterol transport (RCT), HDL possesses anti-oxidative, anti-inflammatory, and anti-apoptotic effects on endothelial cells, exerts anti-migrative and anti-proliferative functions on smooth muscle cells, and presents anti-development and anti-metastasis characteristics on cancer cells [7, 8]. Nevertheless, HDL either modified by oxidation and glycation or isolated from patients with systemic inflammation decreases its

protective effects and even becomes a pro-inflammatory, pro-oxidative, and proapoptotic factor [9]. Consequently, the question whether HDL-C is still the "good cholesterol" becomes more bewildering to be answered.
