Although atherosclerosis has been considered to be multi-factorial disease in which genetic, environmental, metabolic factors have been implicated, the gaps remain in our knowledge of the etiopathogenesis of atherosclerosis. There is mounting evidence that inflammation plays an important role in the initiation, development as well as evolution of atherosclerosis, suggesting that atherosclerosis is an inflammation disease.1,2 Although triggers and pathways of inflammation are probably multiple and different in different clinical settings, the data from animals as well as humans including our groups indicated that an inflammatory process was involved in all stages of atherosclerosis appeared in different clinical entities.